Main components of essential oils with antimicrobial potential.
\\n\\n
More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:{caption:"IntechOpen Maintains",originalUrl:"/media/original/113"}},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
\n'}],latestNews:[{slug:"webinar-introduction-to-open-science-wednesday-18-may-1-pm-cest-20220518",title:"Webinar: Introduction to Open Science | Wednesday 18 May, 1 PM CEST"},{slug:"step-in-the-right-direction-intechopen-launches-a-portfolio-of-open-science-journals-20220414",title:"Step in the Right Direction: IntechOpen Launches a Portfolio of Open Science Journals"},{slug:"let-s-meet-at-london-book-fair-5-7-april-2022-olympia-london-20220321",title:"Let’s meet at London Book Fair, 5-7 April 2022, Olympia London"},{slug:"50-books-published-as-part-of-intechopen-and-knowledge-unlatched-ku-collaboration-20220316",title:"50 Books published as part of IntechOpen and Knowledge Unlatched (KU) Collaboration"},{slug:"intechopen-joins-the-united-nations-sustainable-development-goals-publishers-compact-20221702",title:"IntechOpen joins the United Nations Sustainable Development Goals Publishers Compact"},{slug:"intechopen-signs-exclusive-representation-agreement-with-lsr-libros-servicios-y-representaciones-s-a-de-c-v-20211123",title:"IntechOpen Signs Exclusive Representation Agreement with LSR Libros Servicios y Representaciones S.A. de C.V"},{slug:"intechopen-expands-partnership-with-research4life-20211110",title:"IntechOpen Expands Partnership with Research4Life"},{slug:"introducing-intechopen-book-series-a-new-publishing-format-for-oa-books-20210915",title:"Introducing IntechOpen Book Series - A New Publishing Format for OA Books"}]},book:{item:{type:"book",id:"4645",leadTitle:null,fullTitle:"Biodegradation and Bioremediation of Polluted Systems - New Advances and Technologies",title:"Biodegradation and Bioremediation of Polluted Systems",subtitle:"New Advances and Technologies",reviewType:"peer-reviewed",abstract:"This book contains a collection of research works focused on the biodegradation of different types of pollutants, both in water and solids. The book is divided in three major sections: A) Biodegradation of organic pollutants in solids and wastewater, B) Biodegradation of complex pollutants, and C) Novel technologies in biodegradation and bioremediation.",isbn:null,printIsbn:"978-953-51-2238-8",pdfIsbn:"978-953-51-5418-1",doi:"10.5772/59459",price:119,priceEur:129,priceUsd:155,slug:"biodegradation-and-bioremediation-of-polluted-systems-new-advances-and-technologies",numberOfPages:178,isOpenForSubmission:!1,isInWos:1,isInBkci:!1,hash:"de86e2d98b4cc7ee51ca11a65f08079f",bookSignature:"Rolando Chamy, Francisca Rosenkranz and Lorena Soler",publishedDate:"December 17th 2015",coverURL:"https://cdn.intechopen.com/books/images_new/4645.jpg",numberOfDownloads:19038,numberOfWosCitations:38,numberOfCrossrefCitations:24,numberOfCrossrefCitationsByBook:2,numberOfDimensionsCitations:54,numberOfDimensionsCitationsByBook:2,hasAltmetrics:0,numberOfTotalCitations:116,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"October 15th 2014",dateEndSecondStepPublish:"November 5th 2014",dateEndThirdStepPublish:"February 9th 2015",dateEndFourthStepPublish:"May 10th 2015",dateEndFifthStepPublish:"June 9th 2015",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"165784",title:"Dr.",name:"Rolando",middleName:null,surname:"Chamy",slug:"rolando-chamy",fullName:"Rolando Chamy",profilePictureURL:"https://mts.intechopen.com/storage/users/165784/images/4439_n.jpg",biography:"Rolando Chamy obtained his professional degree in Biochemical Engineering from Pontificia Universidad Catolica de Valparaíso (PUCV), Chile, in 1982. He obtained his PhD in Chemical Engineering from the University of Santiago de Compostela, Spain, in 1991. The same year, he became fulltime Professor in the School of Biochemical Engineering at PUCV. He also participated in the creation of the Biotechnology Center (NBC) of PUCV. Currently, Dr. Chamy serves as the Director of NBC and is the main researcher of the bioenergy unit of Fraunhofer Chile Research. His research interests are in the fields of bioenergy, biofuels, environmental engineering, and climate change. Dr. Chamy has authored and coauthored more than 200 scientific publications.",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"2",totalChapterViews:"0",totalEditedBooks:"4",institution:{name:"Pontificial Catholic University of Valparaiso",institutionURL:null,country:{name:"Chile"}}}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:{id:"252346",title:"Dr.",name:"Francisca",middleName:null,surname:"Rosenkranz",slug:"francisca-rosenkranz",fullName:"Francisca Rosenkranz",profilePictureURL:"https://mts.intechopen.com/storage/users/252346/images/system/252346.jpg",biography:"Francisca Rosenkranz, candidate for PhD in Biotechnology for the program that this house of studies teaches with the Santa María University. Francisca Rosenkranz, who is doing her doctoral thesis in co-tutelage with the University of Santiago de Compostela, Spain.",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"0",institution:null},coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"863",title:"Biodegradation",slug:"biodegradation"}],chapters:[{id:"49070",title:"Fungi in Landfill Leachate Treatment Process",doi:"10.5772/60863",slug:"fungi-in-landfill-leachate-treatment-process",totalDownloads:2109,totalCrossrefCites:4,totalDimensionsCites:10,hasAltmetrics:0,abstract:"The landfill leachate has high concentration of COD, ammonia and other recalcitrant composition compounds. The amount of eachwhich is mainly largely dependent on the age of the landfill. The conventional leachate treatments can be classified as chemical-physical treatments and biological treatments. Using fungi to treat leachate is an emerging research topic. Fungi, with their excellent recalcitrant compound degradability, have been used to treat industrial wastewater that contains toxic or recalcitrant compound. Due to the complex composition and toxicity of landfill leachate, fungi have showed shown better removal efficiency in terms of COD, toxicity and color removal than the conventional leachate treatment. White rot fungi species and yeast are so far the two species that have been studied in treating landfill leachate. Future research should be extended to the other fungi species as well asand also on the impact of ammonia in landfill leachate on the fungi treatment process.",signatures:"Yanan Ren and Qiuyan Yuan",downloadPdfUrl:"/chapter/pdf-download/49070",previewPdfUrl:"/chapter/pdf-preview/49070",authors:[{id:"173704",title:"Dr.",name:"Qiuyan",surname:"Yuan",slug:"qiuyan-yuan",fullName:"Qiuyan Yuan"}],corrections:null},{id:"49735",title:"Culture Condition Effect on Bioflocculant Production and Actual Wastewater Treatment Application by Different Types of Bioflocculants",doi:"10.5772/62114",slug:"culture-condition-effect-on-bioflocculant-production-and-actual-wastewater-treatment-application-by-",totalDownloads:1935,totalCrossrefCites:2,totalDimensionsCites:5,hasAltmetrics:0,abstract:"The effect of culture condition on different types of bioflocculant production and its application on actual wastewater treatment were studied in this chapter. The advantages of mixed strain HXJ-1 were as follows: directly using acidic wine wastewater, adapting to wastewater at high concentrations and the presence of less nitrogen. HXJ-1 achieved good flocculating rate when the chemical oxygen demand (COD) was 12,000 mg/L, C/N 20:1. Three kinds of bioflocculants had some good treatment results on starch wastewater, printing and dyeing wastewater and landfill leachate. The treatment effect of XJBF-1 (produced by mixed strain HXJ-1) on the starch wastewater was better than that of traditional polyacrylamide and other bioflocculants produced by a single bacterial (X15BF-1) and yeast strain (J1BF-1). XJBF-1 had better treatment results on three types of wastewater. It also had good removal rate of chromaticity, especially on the starch wastewater , the printing and dyeing wastewater; the removal rate was up to 88%, and the starch wastewater COD removal rate was up to 86%.",signatures:"Fan Zhang, Wenju Jiang, Xiangdong Wang, Xiujuan Ji, Yina Wang,\nWang Zhang and Jiao Chen",downloadPdfUrl:"/chapter/pdf-download/49735",previewPdfUrl:"/chapter/pdf-preview/49735",authors:[{id:"174018",title:"Ph.D.",name:"Fan",surname:"Zhang",slug:"fan-zhang",fullName:"Fan Zhang"}],corrections:null},{id:"48997",title:"Anaerobic Biodegradation of Solid Substrates from Agroindustrial Activities — Slaughterhouse Wastes and Agrowastes",doi:"10.5772/60907",slug:"anaerobic-biodegradation-of-solid-substrates-from-agroindustrial-activities-slaughterhouse-wastes-an",totalDownloads:2175,totalCrossrefCites:6,totalDimensionsCites:9,hasAltmetrics:0,abstract:"Solid wastes from the meat industry are produced in large amounts resulting in a negative impact on the environment if not properly treated. Due to their high content of proteins and fats, these residues are excellent substrates for anaerobic digestion which holds high potential for methane yield. However, possible toxic compounds may be formed during its biodegradation with a consequent failure of the process under long-term operation. The anaerobic co-digestion of such residues with other co-substrates as those generated in agricultural activities has been proposed as a good alternative to overcome these problems. Nevertheless, today there is very little knowledge to assess on mixture interactions connected to wastes composition, biodegradability, and the kinetics of the anaerobic process when complex materials are utilized in ternary and quaternary mixture, specifically when co-digesting solid cattle slaughterhouse waste with agrowaste. It is therefore important to select the right combination of substrates and ratios to obtain synergy instead of antagonism in those mixtures. This chapter aims to provide an overview of the anaerobic digestion of solid slaughterhouse waste and agrowaste, as well as the influence of mixture interactions on its biodegradation.",signatures:"Ileana Pereda Reyes, Jhosané Pagés Díaz and Ilona Sárvári Horváth",downloadPdfUrl:"/chapter/pdf-download/48997",previewPdfUrl:"/chapter/pdf-preview/48997",authors:[{id:"173935",title:"M.Sc.",name:"Jhosané",surname:"Pagés-Díaz",slug:"jhosane-pages-diaz",fullName:"Jhosané Pagés-Díaz"},{id:"173936",title:"Dr.",name:"Ileana",surname:"Pereda-Reyes",slug:"ileana-pereda-reyes",fullName:"Ileana Pereda-Reyes"},{id:"173990",title:"Dr.",name:"Ilona",surname:"Sárvári Horváth",slug:"ilona-sarvari-horvath",fullName:"Ilona Sárvári Horváth"}],corrections:null},{id:"48965",title:"Organic Matter Biodegradation by Bacterial Consortium under Metal Stress",doi:"10.5772/60980",slug:"organic-matter-biodegradation-by-bacterial-consortium-under-metal-stress",totalDownloads:1874,totalCrossrefCites:0,totalDimensionsCites:2,hasAltmetrics:0,abstract:"Organic matter biodegradation proceeds via multiple enzymatic reactions, involving different oxidants as well as a number of intermediate compounds. Microbial reworking of organic matter can result in a substantial microbial contribution to the total organic matter pool. The investigations of the mechanisms, which can alter the microbial metabolism in marine sediments, are essential for understanding diagenetic processes, especially at those environments with toxic metal concentrations. Metals can bind with cells components, affecting their functioning. Consequently, the organic matter oxidation in the cellular metabolism may be affected. By contrast, the carbon sources are discriminated between labile and refractory organic compounds. The labile portion of organic matter mainly consists of biopolymers and includes carbohydrates, lipids, and proteins. The aim of this chapter is to present the main results of 10 years of studies regarding the organic matter oxidation by bacterial consortia under toxic metal levels on a tropical estuarine environment surrounded in part by mangrove areas. As the main find, the chronic dominance of lipids and carbohydrates at estuaries and mangroves systems may change the bacterial trophic state from aerobic to anaerobic metabolism. This alteration may reflect on decreasing both bacterial efficiency of organic matter degradation and bacterial productivity. Further, when these systems show high levels of metals at the sediment, the metabolic efficiency is even lower because, although bacteria consortia is able to produce extracellular polymeric substances (EPS) as defense mechanism, multimetal contamination may hinder bacterial organic matter oxidation through dehydrogenase activity inhibition.",signatures:"Simone Pennafirme, Inaya Lima, José Bitencourt, Mirian Crapez and\nRicardo Lopes",downloadPdfUrl:"/chapter/pdf-download/48965",previewPdfUrl:"/chapter/pdf-preview/48965",authors:[{id:"59687",title:"Dr.",name:"Ricardo",surname:"Lopes",slug:"ricardo-lopes",fullName:"Ricardo Lopes"},{id:"174456",title:"Prof.",name:"Inaya",surname:"Lima",slug:"inaya-lima",fullName:"Inaya Lima"},{id:"174464",title:"MSc.",name:"Simone",surname:"Pennafirme",slug:"simone-pennafirme",fullName:"Simone Pennafirme"},{id:"174465",title:"Prof.",name:"Mirian",surname:"Crapez",slug:"mirian-crapez",fullName:"Mirian Crapez"},{id:"174467",title:"Dr.",name:"José Augusto Pires",surname:"Bitencourt",slug:"jose-augusto-pires-bitencourt",fullName:"José Augusto Pires Bitencourt"}],corrections:null},{id:"48926",title:"Biodegradation of Paclobutrazol — A Plant Growth Regulator Used in Irrigated Mango Orchard Soil",doi:"10.5772/60818",slug:"biodegradation-of-paclobutrazol-a-plant-growth-regulator-used-in-irrigated-mango-orchard-soil",totalDownloads:1980,totalCrossrefCites:2,totalDimensionsCites:6,hasAltmetrics:0,abstract:"Paclobutrazol (PBZ), [2RS,3RS]-1-[4-chlorophenyl]-4,4-dimethyl-2-(1H-1,2,4-triazol-1-yl) pentan-3-ol, consists of a triazole ring and a benzene ring-chloro linked to a carbon chain open. It is a plant growth regulator widely used in many crops in order to produce fruit throughout the year by inhibiting gibberellin synthesis, a hormone responsible for the vegetative plant growth. Actually, studies are showing that paclobutrazol remains active in the soil for a long time, affecting the growth and development of subsequent crops by reducing plant vigor. Biodegradation is an effective and cheap process that can to degrade or transform contaminants to less toxic or nontoxic. In this work, the biodegradation of paclobutrazol was studied using in submersed culture and saturated and unsaturated soils. In these conditions, experiments with biostimulation and bioaugmentation were performed. In the experiments carried out in submersed culture, with biostimulation by addition of glycerol, the PBZ biodegradation was higher than that with PBZ as sole carbon source. The biodegradation of PBZ in unsaturated soils was more efficient when soil samples with a history of application of PBZ were used. The highest number of applications of PBZ favored biodegradation. The biodiversity of the microbiota in the soil favored the biodegradation of PBZ aromatic rings. PBZ was not seen to be phytotoxic and the biodegraded products increased the germination index.",signatures:"Fernanda Vaz, Ednaldo Santos-Filho, Suzyane Silva, Silvany Araújo,\nThatiana Stamford-Arnaud, Andrea Bandeira, Ana Cristina\nBrasileiro-Vidal, Newton Pereira Stamford, Maria Aparecida Mouco\nand Ester Gouveia",downloadPdfUrl:"/chapter/pdf-download/48926",previewPdfUrl:"/chapter/pdf-preview/48926",authors:[{id:"73324",title:"Prof.",name:"Newton",surname:"Stamford",slug:"newton-stamford",fullName:"Newton Stamford"},{id:"113733",title:"Prof.",name:"Ester",surname:"Gouveia",slug:"ester-gouveia",fullName:"Ester Gouveia"},{id:"160856",title:"Dr.",name:"Ana Christina",surname:"Brasileiro-Vidal",slug:"ana-christina-brasileiro-vidal",fullName:"Ana Christina Brasileiro-Vidal"},{id:"174383",title:"Dr.",name:"Fernanda",surname:"Vaz",slug:"fernanda-vaz",fullName:"Fernanda Vaz"},{id:"174384",title:"MSc.",name:"Ednaldo Amaro",surname:"Santos-Filho",slug:"ednaldo-amaro-santos-filho",fullName:"Ednaldo Amaro Santos-Filho"},{id:"174385",title:"Dr.",name:"Thatiana",surname:"Stamford-Arnaud",slug:"thatiana-stamford-arnaud",fullName:"Thatiana Stamford-Arnaud"},{id:"174386",title:"Dr.",name:"Maria Aparecida",surname:"Mouco",slug:"maria-aparecida-mouco",fullName:"Maria Aparecida Mouco"},{id:"175594",title:"BSc.",name:"Suzyane",surname:"Silva",slug:"suzyane-silva",fullName:"Suzyane Silva"},{id:"175595",title:"Dr.",name:"Andrea",surname:"Bandeira",slug:"andrea-bandeira",fullName:"Andrea Bandeira"},{id:"175596",title:"BSc.",name:"Silvany",surname:"Araújo",slug:"silvany-araujo",fullName:"Silvany Araújo"}],corrections:null},{id:"48964",title:"Biodegradation of Aromatic Compounds",doi:"10.5772/60894",slug:"biodegradation-of-aromatic-compounds",totalDownloads:3216,totalCrossrefCites:5,totalDimensionsCites:8,hasAltmetrics:0,abstract:"Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous persistent environmental contaminants generated by natural combustion processes and human activities. PAHs are considered hazardous because of cytotoxic, mutagenic, and carcinogenic effects. Sixteen individual PAH compounds have been identified as priority pollutants by the United States Environmental Protection Agency (U.S. EPA). All substances originated in to the environment by either biogenic or anthropogenic sources. Anthropogenic compounds describe synthetic compounds, and compound classes as well as elements and naturally occurring chemical entities which are mobilized by man’s activities. In the marine environment, the fate of pollutants is largely determined by biogeochemical process. Some of these chemical changes enhance the toxicity of the pollutants. Other chemical changes cause the degradation or immobilization of pollutants and, as a result, act to purify the waters. Possible fates for PAHs, released into the environment, include volatilization, photo-oxidation, chemical oxidation, bioaccumulation and adsorption on soil particles, leaching, and microbial degradation. Elevated concentrations of polycyclic aromatic hydrocarbons (PAHs) have been found in mangrove sediments due to anthropogenic compounds.",signatures:"Mehdi Hassanshahian, Moslem Abarian and Simone Cappello",downloadPdfUrl:"/chapter/pdf-download/48964",previewPdfUrl:"/chapter/pdf-preview/48964",authors:[{id:"163666",title:"Dr.",name:"Mehdi",surname:"Hassanshahian",slug:"mehdi-hassanshahian",fullName:"Mehdi Hassanshahian"}],corrections:null},{id:"48996",title:"Advantages and Limitations of Using FTIR Spectroscopy for Assessing the Maturity of Sewage Sludge and Olive Oil Waste Co-composts",doi:"10.5772/60943",slug:"advantages-and-limitations-of-using-ftir-spectroscopy-for-assessing-the-maturity-of-sewage-sludge-an",totalDownloads:2869,totalCrossrefCites:5,totalDimensionsCites:14,hasAltmetrics:0,abstract:"Composts prepared using different solid and liquid organic wastes from various sources can be used as growing media when these materials present adequate proprieties for plant development. The stability and maturity are among the main characteristics of composts. The purpose of this study is to recommend specific bands of the IR spectrum recorded on different composts to enable qualitative and rapid monitoring of the stages of biodegradation during composting. At the beginning of humification, the significant decrease in the intensity of the band located at 1735 cm–1 shows that lignin is affected at the first stage of the composting process. At the end of the humification, the band located toward 3450–3420 cm–1 at the beginning of the process undergoes a systematic shift (Δν of the order of 10 cm–1) toward lower wave numbers. The band located at 1660–1650 cm–1 on the Fourier transform infrared spectroscopy (FTIR) spectra before composting shifts systematically toward 1640 cm–1 at the end of humification. This phenomenon can be used as index of compost maturity. Measuring the band at 1035 cm–1 as an internal standard, it is possible to quantify the degradation rate of organic matter.",signatures:"Loubna El Fels, Mohamed Zamama and Mohamed Hafidi",downloadPdfUrl:"/chapter/pdf-download/48996",previewPdfUrl:"/chapter/pdf-preview/48996",authors:[{id:"164092",title:"Prof.",name:"Mohamed",surname:"Hafidi",slug:"mohamed-hafidi",fullName:"Mohamed Hafidi"},{id:"175610",title:"Dr.",name:"Loubna",surname:"El Fels",slug:"loubna-el-fels",fullName:"Loubna El Fels"},{id:"175611",title:"Prof.",name:"Mohamed",surname:"Zamama",slug:"mohamed-zamama",fullName:"Mohamed Zamama"}],corrections:null},{id:"49732",title:"Biodegradation of Petroleum-Polluted Soils Using CNB-Tech – The Nigerian Experience",doi:"10.5772/62116",slug:"biodegradation-of-petroleum-polluted-soils-using-cnb-tech-the-nigerian-experience",totalDownloads:2883,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"Remediation of petroleum-hydrocarbon-polluted soil via biodegradation process is viewed globally as an environmentally friendly process. In this study, an overview of past and present field-scale petroleum hydrocarbon biodegradation techniques utilized in Nigeria was conducted using the tools of literature review and field survey. Pilot-scale biodegradation of hydrocarbons in petroleum-impacted clay soil of up to 42-year-long contamination using novel and eco-safe CNB-Tech was carried out. This was followed by a comparative evaluation of crop growth performance on crude-oil-polluted soil remediated using a biodegradation technique adopted by a reputable oil company in Nigeria and the innovative CNB-Tech. The study revealed that CNB-Tech is an innovative, time-effective, cost-effective and eco-friendly bioremediation technique and has the potential to excel over some existing biodegradation procedures employed by many oil industries especially in the developing countries.",signatures:"Iheoma M. Adekunle, Nedo Osayande and Temitope T. Alawode",downloadPdfUrl:"/chapter/pdf-download/49732",previewPdfUrl:"/chapter/pdf-preview/49732",authors:[{id:"77235",title:"Dr.",name:"Iheoma Mary",surname:"Adekunle",slug:"iheoma-mary-adekunle",fullName:"Iheoma Mary Adekunle"}],corrections:null}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},subseries:null,tags:null},relatedBooks:[{type:"book",id:"3569",title:"Biodegradation",subtitle:"Life of Science",isOpenForSubmission:!1,hash:"bb737eb528a53e5106c7e218d5f12ec6",slug:"biodegradation-life-of-science",bookSignature:"Rolando Chamy and Francisca Rosenkranz",coverURL:"https://cdn.intechopen.com/books/images_new/3569.jpg",editedByType:"Edited by",editors:[{id:"165784",title:"Dr.",name:"Rolando",surname:"Chamy",slug:"rolando-chamy",fullName:"Rolando Chamy"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3540",title:"Biodegradation",subtitle:"Engineering and Technology",isOpenForSubmission:!1,hash:"0ee069d311f4d412f6bbf7180e3a8ea4",slug:"biodegradation-engineering-and-technology",bookSignature:"Rolando Chamy and Francisca Rosenkranz",coverURL:"https://cdn.intechopen.com/books/images_new/3540.jpg",editedByType:"Edited by",editors:[{id:"165784",title:"Dr.",name:"Rolando",surname:"Chamy",slug:"rolando-chamy",fullName:"Rolando Chamy"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3570",title:"Biodegradation of Hazardous and Special Products",subtitle:null,isOpenForSubmission:!1,hash:"29ce0f4a059cb02b060a2b4082ca81e0",slug:"biodegradation-of-hazardous-and-special-products",bookSignature:"Rolando Chamy and Francisca Rosenkranz",coverURL:"https://cdn.intechopen.com/books/images_new/3570.jpg",editedByType:"Edited by",editors:[{id:"165784",title:"Dr.",name:"Rolando",surname:"Chamy",slug:"rolando-chamy",fullName:"Rolando Chamy"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3426",title:"Organic Pollutants",subtitle:"Monitoring, Risk and Treatment",isOpenForSubmission:!1,hash:"4dafb52ed4f5e21f079ab4b2f6825e78",slug:"organic-pollutants-monitoring-risk-and-treatment",bookSignature:"M. 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The essential oils are formed by volatile substances and generally have low molecular weight, these substances are formed in the secondary metabolism of aromatic plants [1, 2]. However, some natural factors such as physiological variations, environmental conditions, geographic variations, genetic factors and plant evolution can alter the chemical composition of these oils as well as their yield [3].
\nThe extraction of essential oils usually occurs with the use of conventional techniques such as hydrodistillation using a Clevenger type extractor, which is the most widespread technique for the isolation of volatile plant oils [4, 5], however, other extraction techniques are also efficient such as extraction with supercritical CO2 [6, 7], this type of extraction is a technique considered clean and does not cause change in the chemical structures of the molecules, since it usually works at low operating temperatures [8].
\nIn nature, essential oils play an important role in plants as protection and communication, chemical protections that these secondary metabolites present, also is decisive in plant resistance against pathogens and herbivores [9]. In the communication the plant can use a chemical agent that travels through the atmosphere and activate defensive genes of other plants, such as the methyl jasmonate of
In the industry these oils are widely studied, mainly for their potential applications as agents promoting biological activities. The volatile compounds have presented over the years several pharmacological applications, such as antioxidant, anticancer, antiprotozoal, antimicrobial and anti-inflammatory activities [11, 12, 13, 14, 15]. In recent work [16] demonstrated that species like
The antimicrobial action of essential oils is not yet fully understood, but can be attributed to their permeability to the cell wall of microorganisms due to their diverse chemical and synergistic composition. The hydrophobic characteristic of the essential oils acts in the partition of the lipids of the cellular membrane and the mitochondria, making them more permeable, in this way, the critical ions and molecules (lipids, proteins and nucleic acids) are extravasated, leading them to death. EOs generally have less action on gram-positive bacteria than on gram-negative bacteria due to the interaction of the hydrophobic components of the essential oils and the cell membrane [19, 20, 21].
\nDifferent methods are used to evaluate the antibacterial and antifungal properties. The most used are: the method of disc diffusion of Agar, Minimal Inhibition Concentration (MIC), Minimum Bacteria Concentration (MBC) and Minimum Fungicide Concentration (MFC). Since the use of the disc diffusion method in agar is limited by the hydrophobic nature of essential oils and plant extracts that prevents its uniform diffusion through the agar medium, most authors report the results obtained with MIC and MBC [22].
\nIn recent years, different microbial species of medical interest have been tested, from which encouraging results have emerged. Table 1 shows data on the antimicrobial activity of essential oils on fungi and bacteria, also showing the main components of essential oil.
\nPlant source | \nMain components | \nMicroorganism | \n*MIC | \nReference | \n
---|---|---|---|---|
β-Pinene; eucalyptol; linalool; coronarin-E; α-pinene; p-cymene; γ-terpinene and 10- | \n3.12–400 μg/ml | \n[23] | \n||
Methyl salicylate; fenchol; 1,2-cyclohexanedione dioxime; 1,4-octadiene and linalool | \n50–200 mg/ml | \n[24] | \n||
β-caryophyllene Germacrene D Spathulenol | \n1500–3000 μg/ml | \n[25] | \n||
Caryophyllene oxide Iridodial β-monoenol Acetate | \n1000–3000 μg/ml | \n|||
β-Caryophyllene β-Sesquiphellandrene Caryophyllene oxide | \n1000–3000 μg/ml | \n|||
β-Sesquiphellandrene Actinidine Germacrene D | \n1000–3000 μg/ml | \n|||
α-Pinene β-Pinene β-Caryophyllene germacrene D limonene | \n15.62–62.50 μg/ml | \n[26] | \n
Main components of essential oils with antimicrobial potential.
Minimum Inhibitory Concentrations.
The potential antimicrobial activity of essential oils of the
Essential oils isolated from
The good results obtained encourage future research aimed at a possible application of these substances in food, pharmaceutical and cosmetology fields. Table 1 presents the main chemical components of essential oils of several plants with antimicrobial potential.
\nThe interest in the study of the antioxidant substances of essential oils has become more and more intensified and is now indispensable for the prevention of diverse pathologies [27]. In the literature, it is reported the presence of antioxidant activity in several essential oils [28, 29, 30].
\nThis property acts at different levels in the microorganism protection and plays a key role in some of the biological activities of essential oils, being able to combat the development of oxidative stress that causes damage to health, increasing the risk of diseases such as Alzheimer’s, Parkinson’s and inflammation associated with atherosclerosis and rheumatoid arthritis. Some studies point out that these diseases may be consequences of damages caused by free radicals, besides oxygen and reactive nitrogen species that act as mediators of inflammation as messenger molecules. This shows that essential oils can also act as an anti-inflammatory agent [31, 32, 33].
\nEssential oils have great potential in the nutrition industry in view of their antioxidant properties, they are use as feed additives for farm animals, for example, and that may be fundamental to the quality of food products from these animals, since essential oils can improve nutritional value, oxidative stability and increase the shelf life of these products such as meats and eggs. In addition, they are often treated as foods to enhance the taste and organoleptic properties, and even has the function of decreasing the process of deterioration of food. The latter is mainly due to its antimicrobial and antioxidants activities [31, 34, 35].
\nThe interest in extracts rich in natural antioxidants has recently increased, especially the antioxidant activity of essential oils. Most of them confirm the assumption that essential oils are promising as natural antioxidants, which can replace synthetic additives such as butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) that are potentially harmful to human health [36, 37, 38]. In this context, Table 2 presents some more recent studies found in the literature based on the antioxidant activity of essential oils, highlighting its main constituents and antioxidant performance evaluation methods.
\nPlant source | \nMain constituents | \nBiological activity | \nReference | \n
---|---|---|---|
α-Pinene, bornyl acetate, β-caryophyllene, α-guaiene, germacrene D | \n[39] | \n||
Linalool, methyl chavicol, 1,8-cineole | \nThe free radical scavenging activity of the oil was measured by the DPPH method | \n[40] | \n|
Carvone, methyl chavicol, trans-anethole, limonene | \nThe evaluation of the ability to eliminate the free radicals of the oils was by the DPPH and ABTS methods | \n[41] | \n|
Camphor, 1,8-cineole, camphene, α-pinene | \nThe | \n[42] | \n|
α-Pinene, 1,8-cineole, Camphor | \nThe antioxidant activity was evaluated in 7 samples of rosemary oil based on the measurement of the antioxidant reduction capacity in relation to the DPPH radical | \n[43] | \n
Antioxidant activity of essential oils.
Essential oils from aromatic plants have been treated as a product containing anticancer properties because they have the ability to inhibit cell proliferation and decrease the spread of cancer, improving the quality of life of cancer patients and reducing the level of their agony. Mediated therapy with essential oils can be used in combination with conventional therapies in the treatment of cancer (quimioterapia e radioterapia) [44, 45, 46].
\nAccording to the World Health Organization [47] cancer is a generic term used for a large group of diseases that can affect any part of the body, is characterized by the growth of abnormal cells beyond their usual limits in the body. Other common terms used are malignant tumors and neoplasms, the latter process or stage of the disease is called metastasis. Cancer is a major public health problem and is considered the second leading cause of death worldwide, accounting for 8.8 million deaths by 2015, where nearly 1 in 6 deaths is caused by cancer. Ref. [48] reported that the American Cancer Society reported in the year 2017 approximately 1,688,780 new cases of cancer and 600,920 deaths from cancer in the United States. According to [49, 50, 51] the most common causes of cancer death are melanoma, leukemia, followed by lung, liver, prostate, breast, cervical, colorectal, and endometrial cancers.
\nThe sharp increase in the number of cancer cases can be attributed to eating habits, since foods contain many chemicals such as preservatives and dyes, making people more susceptible to cancer, which can also be accentuated with the use of tobacco and alcohol, chronic infections, exposure to harmful radiation, or due to change in lifestyle and environmental pollution [45, 52]. Previous studies have reported that oxidative stress increases the onset of different chronic diseases, including cancer. Reactive oxygen species (ROS) are highly unstable compounds that have the ability to attack cells and tissues in the human body, followed by destructive effects that lead to the beginning of cancer [46, 53].
\nTherefore, there has been a recent increase in the use of natural products such as spices and plants to replace or accompany common treatments for cancer because of their high costs, side effects and the development of resistance of patients against anticancer drugs [44, 52].
\nThus, essential oils from different aromatic plants have anticancer potential against mouth, breast, lung, prostate, liver, kidney, colon, bone, ovary, pancreas, uterus and brain cancer and even in leukemia, glioblastoma, melanoma [45, 54]. Thus [52] have shown that essential oil extracted from cloves (
The myrtle essential oil (
Essential oils act in the chemoprevention and suppression of cancer, which involve apoptosis, cell cycle retention, antimetastatic and antiangiogenic, increased levels of reactive oxygen and nitrogen species (ROS/RNS), modulation of DNA repair and others that demonstrate their antiproliferative cancer cell activity [53, 57]. In addition, the lipophilic nature of the EOs allows them to cross cell membranes and enter easily within the cell [45, 54], in Table 3 we can observe the anticancer activities of different aromatic plants.
\nPlant source | \nMain constituents | \nBiological activity | \nReference | \n
---|---|---|---|
Nerol, kaempferol and geraniol | \nLiver cancer, human breast cancer, prostate cancer | \n[58] | \n|
4,5-dimetiltiazol-2-il and 2,5-difeniltetrazólio | \nBreast cancer | \n[55] | \n|
d-Limonene and alcohol perylic (oxygenated monoterpene) | \nColorectal/colon cancer, prostate cancer, lung cancer | \n[46] | \n|
β-Caryophyllene, 1-phenanthrenecarboxylic acid, α-caryophyllene and azulene benzenedicarboxylic acid | \nColorectal/colon carcinoma, pancreatic cancer | \n[59] | \n|
1,8-cineole, linalool, myrtenyl acetate and myrtenol | \nBlood cancer (leukemia) | \n[56] | \n|
Pulegol, citronellol and citronellil acetate | \nBreast cancer, liver cancer, colorectal/colon cancer | \n[53] | \n|
Cinnamic aldehyde, cinnamyl aldehyde and tannins | \nHead and neck cancer | \n[57] | \n|
Betulinic acid and triterpenes | \nHuman breast cancer | \n[52] | \n|
γ-Terpinene, timol and P-cymene | \nLiver cancer | \n[60] | \n|
2-cyclohexen-1-one and 4-ethynyl-4-hydroxy-3,5,5-trimethyl | \nLiver cancer, cervical cancer | \n[61] | \n|
Hydrocarbons, monoterpene, oxygenated monoterpenes sesquiterpene and diterpenes | \nHuman breast cancer, prostate cancer, kidney cancer | \n[62] | \n|
cis-β-ocimene, cis-tagetone and trans-tagetenone | \nBreast cancer, blood cancer (leukemia) | \n[63] | \n
Anticancer activity of essential oils.
Current treatment media control most diseases of protozoan origin mainly through chemotherapy, where synthetic drugs are generally used, but they show several side effects of cytotoxicity in humans. Due to the hydrophobic and bioactivities nature of its components, essential oils (EO) can be considered important sources of development of agents against intracellular pathogens such as protozoa, which cause parasitic diseases [64].
\nThe EO of leaves of
Another EO that presents the antimalarial effect is that obtained from
The EO of the leaves of
The antiparasitic activity of
The anthelmintic activity of
Plant source | \nMain constituents | \nBiological activity | \nReference | \n
---|---|---|---|
Ascaridole, carvacrol and caryophyllene oxide | \nAntileshmanial, antimalarial and antitrypanosoma | \n[72] | \n|
(E)-cinnamaldehyde and eugenol | \nAntitrypanosoma | \n[73] | \n|
Sesquiterpenes, curzerene, γ-elemene and trans-β-elemenone | \nAntileshmanial | \n[74] | \n|
Borneol, epi-d-muurolol, d-bisabolol, precocene I and eucalyptol | \nAntischistosomatic | \n[75] | \n|
Safrole | \nAntiamoebicidal | \n[76] | \n|
δ-Cadinene, δ-cadinol, β-eudesmol, γ-gurjunene and cedrene | \nAntiamoebicidal | \n[77] | \n
Anti-parasitic activity of essential oils.
Essential oils have complex mixtures of chemicals that are present in different concentrations, these oils are used in medicine to treat a myriad of diseases because they present potential for anti-inflammatory activity [78, 79].
\nInflammation is typically a protective mechanism that can be stimulated by a variety of harmful agents, which may be chemical, physical or biological. Living and vascular tissues respond to stimuli that are considered irritating to the body. These irritations can usually be linked to pain, redness (erythema), heat, tumor (edema), tissue loss or organic function [80, 81].
\nIn recent years the anti-inflammatory potential of essential oils and their chemical position has become the object of study of several researchers in the search for new drugs of natural origin [82, 83, 84], as well as a study of the synergistic anti-inflammatory effect of the chemical constituents of essential oils and synthetic drugs, showing a possible association between clinical remedies with natural products as a pharmacological alternative and avoiding adverse reactions caused by synthetic products [85]. In vivo tests performed on rats confirm the potential of these essential oils as natural products, helping to advance research [86, 87].
\nThe knowledge of the chemical composition and the chemootype of the aromatic plants are important factors in studies of the anti-inflammatory activity, since the concentration of the compounds diverge due to this biological variation, in this way researchers have evaluated both aspects [88, 89]. Evaluating the specific constituents of a particular essential oil may help in understanding the performance of these compounds in the anti-inflammatory action [90]. Table 5 shows the anti-inflammatory potential of different essential oils.
\nPlant source | \nMain constituents | \nBiological activity | \nReference | \n
---|---|---|---|
β-Eudesmol, (E)-β-caryophyllene, caryophyllene oxide, T-muurolol | \nAnti-inflammatory | \n[91] | \n|
β-Pinene, longiborneol, α-pinene, (E)-caryophyllene | \nAnti-inflammatory | \n[84] | \n|
Isoelemicinb, caryophyllene oxide, α-Cadinol, 2-isopropyl benzoic acid | \nAnti-inflammatory | \n[92] | \n|
1,8-Cineole, camphor, β-pinene, E-β-caryophyllene | \nAnti-inflammatory | \n[93] | \n|
Thymol, carvacrol, p-cymene, α-pinene | \nAnti-inflammatory and healing activity | \n[94] | \n|
Limonene, β-pinene, γ-terpinene, sabinene | \nAnti-inflammatory | \n[95] | \n|
Geranial, neral, β-myrcene, geranyl acetate | \nAnti-inflammatory | \n[96]. | \n|
α-Phellandrene, limonene, dill ether, α-pinene | \nAnti-inflammatory | \n[97] | \n|
Linalool, linalylacetate, nerolidol, Z,E-farnesol | \nAnti-inflammatory | \n[98] | \n|
Borneol, caryophyllene, ledol, caryophyllene oxide | \nAnti-inflammatory | \n[99] | \n
Anti-inflammatory activity of essential oils.
Essential oils may play an important role in the maintenance of human health, since they have several biological properties, and may become a natural alternative for the control of several diseases, however, the great majority of published works present the results of these oils based on its chemical composition complex and not only based on a substance, because the biological effects of these oils can be related to a synergism and/or an antagonism between the chemically active substances that are part of its composition.
\nOliveira M. S (Process Number: 1662230) thank CAPES for the doctorate scholarship.
\nIntracellular and blood potassium levels have crucial effects on cardiovascular system homeostasis. At the most fundamental level, the potassium concentration gradient across cardiac muscle cell (cardiomyocyte) cell membranes is a chief determinant of cardiomyocyte resting membrane potentials. Indeed, disruptions to this concentration gradient (e.g. via increasing or decreasing extracellular blood potassium levels) can lead to altered cardiomyocyte contractility and excitability. Potassium is also vasoactive, with different effects at different extracellular concentrations. At low (5-8 mM) to moderate (8-16 mM) extracellular levels, potassium relaxes the smooth muscle in blood vessel walls by promoting hyperpolarization of vascular smooth muscle. However, at higher levels (16-25 mM and above) (e.g. cardioplegic concentrations), potassium promotes vasoconstriction by facilitating depolarization. Moreover, potassium is released by vascular endothelial cells in response to various chemical mediators and shear stress, thereby contributing to the action of endothelium-derived hyperpolarizing factor [1]. For all of these reasons and more, keeping track of daily potassium intake is often recommended as a lifestyle modification for chronic cardiovascular diseases such as hypertension.
Harnessing the pivotal role of potassium in cardiovascular physiology has proved quite useful for cardiovascular surgery, namely in the form of hyperkalemic (high potassium) cardioplegia. Indeed, throughout the past several decades, a large body of research has testified to the ability of externally administered hyperkalemic solutions to arrest cardiac contractility [2]. This, in conjunction with the development of cardiopulmonary bypass (CPB, also known as the “heart-lung machine”), revolutionized cardiac surgery [3]. These days, many highly invasive procedures like coronary artery bypass grafting are routine with minimal risk of postoperative mortality.
However, hyperkalemic cardioplegia is not without its consequences. Hyperkalemic cardioplegia and reperfusion following CPB have been associated with perioperative and postoperative tissue damage and microvascular dysfunction across several different vascular beds. Moreover, hyperkalemic cardioplegia is also associated with postoperative myocardial dysfunction and reduced cardiac output. Furthermore, blood potassium abnormalities after hyperkalemic cardioplegia-reperfusion, chiefly hypokalemia (but also hyperkalemia, to a lesser degree) are common postoperative challenges in the cardiac ICU. Both abnormalities significantly elevate the risk of arrythmias and, if not managed properly, cardiac arrest and sudden death.
This chapter will discuss the basics of potassium cardioplegia with an emphasis on clinical relevance, beginning with a brief history. Subsequent sections will elaborate on the basic physiology, before considering several perioperative and postoperative adverse effects of hyperkalemic cardioplegia. When possible, information about treatment and clinical management is included. The chapter will conclude with a brief mention of up-and-coming alternatives to hyperkalemic cardioplegia.
As early as the late 1800s, physiologists were starting to become aware of the ability of potassium compounds to arrest cardiac contractility, beginning with individuals like Sidney Ringer who observed that potassium chloride froze the heart in diastole and calcium stimulated the heart during systole [2]. Moving into the start of the 20th century, further investigations revealed associations between high serum potassium and cardiac arrest following ventricular fibrillation; studies also revealed associations between cardioplegia and restoration of sinus rhythm following coronary artery administration of potassium chloride solution and subsequent washout [2]. However, in most of these cardioplegic experiments (often conducted in dogs), refractory ventricular fibrillation and post-procedure reperfusion damage to the myocardium limited discussion of the clinical usefulness of these findings.
During the 1950s, British physician Dennis Melrose hypothesized that the problem with potassium chloride cardioplegia was chloride; therefore, he created a cardioplegic solution using potassium citrate, and tested it on a canine model of cardiopulmonary bypass [4]. Injection of the “Melrose solution”, of potassium citrate plus warm oxygenated whole blood in a 9:1 blood:potassium ratio, into the aortic roots of hypothermic dogs, produced near-immediate cardiac arrest. Reperfusion and washout of cardioplegic solution resulted in restoration of heart function to pre-procedure levels [2]. Within a few years, the Melrose group successfully induced potassium citrate cardioplegia in humans.
Unfortunately, future studies would reveal that in many cases, the Melrose potassium citrate solution still produced post-cardioplegia ventricular fibrillation and myocardial dysfunction [5]. This led to a general pause in clinical application of potassium cardioplegia between the 1960s and early 1980s, in favor of other options mostly involving induction of hypothermic cardiac arrest, which turned out to be no better with respect to postoperative damage than the Melrose solution.
Eventually, research into techniques for potassium cardioplegia would pick up again, and the result would be development of novel solutions for cardioplegia and intraoperative organ preservation. Numerous studies in animal models have validated the principles of diastolic cardiac arrest due to depolarizing potassium cardioplegia [2, 3, 6, 7, 8, 9, 10]. In addition, invention and refinement of heart-lung machines to accompany cardioplegia in the operative room (CPB) opened many new possibilities for cardiac surgery. Today, potassium cardioplegia is an integral tool for cardiac surgeons performing a variety of highly invasive procedures such as coronary artery bypass grafting and aortic valve replacements.
Despite variability in composition, delivery, and temperature, most cardioplegic solutions in use today involve some level of potassium chloride as the main inducer of cardiac arrest, along with ions such as magnesium, low-dose calcium and bicarbonate, the latter of which is particularly important for controlling solution pH [6]. The “original” hyperkalemic cardioplegic solution was the Melrose formula of the 1950s that was discussed earlier, consisting of potassium citrate and warm blood in a 9:1 blood:potassium ratio. However, due to the high incidence of postoperative complications including ventricular fibrillation, this solution is no longer in major clinical use.
In general, cardioplegic solutions fall under two broad umbrellas: crystalloid vs. blood, and warm vs. cold (Table 1). Two crystalloid cardioplegic solutions worth noting are the Custodiol (also known as Bretschneider) and St. Thomas solutions [7]. The St. Thomas solution, introduced first by Hearse and colleagues in 1975, is an example of a short acting cardioplegic solution involving potassium chloride concentrations between 10 and 30 mM [8]. In general, the St. Thomas solution requires repeat dosing, roughly every 20 minutes, to sustain cardioplegia for long durations [7, 9]. Furthermore, myocardial acidosis has been noted between doses of St. Thomas solution [10].
St. Thomas Cardioplegia | Custodiol Cardioplegia | Del Nido Cardioplegia | Buckberg Cardioplegia | Warm Calafiore Cardioplegia (one variant) | |
---|---|---|---|---|---|
K+ | 16 mM | 9 mM | 26 mM | Cold induction: 36 mM Maintenance: 36 mM Reperfusion: 15 mM | 18–20 mM for inducing arrest, repeat delivery every 20 min with decreasing K concentrations |
Ca | 1.2 mM | 0.015 mM | 1.3 mM | ||
Mg | 16 mM | 4 mM | 2 g of 50% magnesium sulfate | 15.5 mM | |
Na | 110 mM | 15 mM | |||
NaHCO3 | 10 mM | 13 mM | |||
Other Components | 18 mM Histidine hydrochloride 18 mM histidine 2 mM tryptophan 30 mM mannitol 1 mM potassium hydrogen 2-ketoglutarate | 13 mL of 1% lidocaine 3.2 g/L of 20% mannitol | 62.5 mL glutamate/aspartate | 500 mL 5% dextrose 4 mM tris(hydroxymethyl)aminomethane Core body temperature maintained at 37 degrees Celsius | |
Blood vs. Crystalloid | Crystalloid | Crystalloid | 4:1 crystalloid: blood ratio | 4:1 crystalloid: blood ratio | Normothermic blood |
Composition of common potassium-based cardioplegic solutions.
In contrast, the Custodiol solution is a form of long acting, single dose cardioplegia consisting primarily of potassium chloride, sodium chloride, and magnesium sulfate as the chief electrolytes [11]. Additional components of the Custodiol solution include tryptophan (membrane stabilization) and histidine buffer (to maintain pH and buffer against byproducts of anaerobic glycolysis that build up during cardioplegia). Curiously, the relatively low levels of potassium (9 mM) and sodium (15 mM) in Custodiol appear to induce cardioplegia through a form of hyperpolarized arrest as opposed to depolarized arrest, unlike most other potassium cardioplegic solutions that have potassium concentrations in the range of 16-36 mM and sodium concentrations in the range of 10-110 mM (see Table 1 for detailed solution ion concentrations).
The general rationale for blood-based cardioplegia has centered on the theory that cardioplegic solutions containing blood are more “physiologic” than crystalloid solutions. For example, blood can support aerobic respiration and may be able to preserve normal myocardial metabolism during surgery. Therefore, blood cardioplegia may reduce the negative consequences of prolonged ischemia during CPB [11]. However, insufficient evidence exists currently to verify that hypothesis, and so any purported advantages of blood over crystalloid cardioplegia are for the time being mainly speculative.
Three hyperkalemic cardioplegic solutions in clinical use that contain blood are the Del Nido, Buckberg, and Calafiore solutions. The Del Nido solution uses a crystalloid:blood ratio of 4:1, and like the Custodiol solution is a long-acting cardioplegic solution, with one dose of 20 ml/kg providing myocardial protection for up to 60–90 minutes [7, 12]. Chief ionic ingredients include potassium chloride for rapid depolarized arrest, sodium bicarbonate to scavenge protons and buffer intracellular pH, and magnesium to block calcium channels and prevent intracellular calcium accumulation during cardioplegic arrest, thereby promoting postoperative myocardial recovery [12, 13]. Lidocaine in the Del Nido solution acts as a sodium channel blocker to mitigate against the sodium “window current” and reduce intracellular sodium accumulation [14].
Buckberg’s cardioplegia is a dextrose and saline-based solution that, similar to the Del Nido solution, consists of a crystalloid:blood ratio of 4:1 [15]. Other components include potassium chloride as the primary depolarizing agent, a tromethamine buffer, and citrate phosphate double dextrose to serve as a calcium chelator. However, unlike the Del Nido solution, Buckberg cardioplegia must be given as three separate formulations, some of which must be administered in multiple doses [15]. First, an induction solution stops the heart, and additional infusions of induction solution must be given every 15 to 20 minutes throughout the procedure. Second, a maintenance solution must be administered to sustain cardiac arrest and provide oxygen and nutrients to the cardiomyocytes. Finally, a reperfusion solution containing glutamate and aspartate is administered prior to removal of the aortic cross clamp to provide the heart with nutrients prior to restarting myocardial contractions.
Calafiore cardioplegia differs from Buckberg and Del Nido in that blood forms the sole foundation of Calafiore cardioplegic solution [16]. Indeed, the original rational proposed by Calafiore et al. was that blood alone, without any crystalloid component, contained everything necessary to prevent ischemia–reperfusion damage. Therefore, simply administering a cardioplegic solution consisting of blood plus extra potassium would be enough to safely stop and later, restart the heart [16]. Moreover, unlike most other forms of cardioplegia in use, the original Calafiore solution was normothermic throughout administration; however, some subsequent variations of Calafiore cardioplegia have used cold blood [16, 17].
Most current methods for administering cardioplegic solutions involve cold cardioplegia, most often cold crystalloid solutions delivered after reducing core body temperature to hypothermic levels [18]. For example, the induction and maintenance solutions for Buckberg cardioplegia are delivered at 4 degrees Celsius after cooling core temperature to below 30 degrees Celsius, with reperfusion solution delivered at 37 degrees Celsius [15]. Similarly, del Nido and Custodiol cardioplegia are often given at 4 degrees Celsius after induction of systemic hypothermia [15, 19].
This practice stems from experimental evidence suggesting that mild hypothermia can protect the myocardium from ischemic damage during cardioplegia [20]. Hypothermia reduces the basal metabolic rate of the heart, which in turn reduces oxygen consumption—an effect augmented by potassium-induced arrest during hyperkalemic cardioplegia [21]. A variety of potential mechanisms may be at play. In animal models of cardiac arrest, mild hypothermia (32–35 degrees Celsius) has been shown to reduce post-arrest infarct size, possibly through various signal transduction pathways, such as Akt and mTOR signaling, both of which are altered during the course of hypothermia [20]. Another potential cardioprotective mechanism of hypothermia may be reduced phosphorylation of various mitogen activated protein kinases (MAPK) like ERK1/2 that normally activate pro-inflammatory mediators like COX-2 (arachidonic acid metabolism) [18]. In general, many details concerning mechanisms of hypothermic myocardial protection during cardioplegia remain to be elucidated.
However, cold hyperkalemic cardioplegia may also inhibit myocardial enzymes that are important for the metabolic and functional recovery of the heart after surgery [22, 23]. Moreover, sustained systemic hypothermia (especially at temperatures below 20 degrees Celsius) during cardiac surgery has also been associated with ventricular fibrillation after rewarming [21]. Given these negative consequences, an increasing amount of attention has been given to the possibility of warm hyperkalemic cardioplegia, primarily warm blood hyperkalemic cardioplegia. Unlike cold hyperkalemic cardioplegic solutions, warm cardioplegic solution is typically administered at between 30 and 35 degrees Celsius under normothermic, as opposed to hypothermic, CPB [24]. Potential advantages of warm blood hyperkalemic cardioplegia over cold crystalloid may include improved myocardial restoration, reduced intracellular swelling, improved membrane stabilization, and reduced hypoxic red blood cell deformation [25].
Of course, warm hyperkalemic cardioplegia is not without its own consequences. Some studies have reported increased likelihoods of perioperative strokes and encephalopathy [26]. Moreover, warm hyperkalemic cardioplegia may contribute to vasodilation during cardiopulmonary bypass, requiring increased use of alpha agonists during operation to maintain stable arterial perfusion pressures [25]. There are also several variations of warm cardioplegia; one common technical variant is “hot shot” cardioplegia, which involves warm induction and subsequent cold cardioplegia, followed by a warm reperfusion [27].
Comparing the effectiveness of warm vs. cold hyperkalemic cardioplegia remains an inconclusive subject of intense debate. A meta-analysis by Fan et al., reported no differences between length of stay, stroke incidence, and atrial fibrillation between patients undergoing warm vs. cold cardioplegia [28]. However, warm cardioplegia correlated with better postoperative cardiac indices and lower peak creatine kinase MB concentrations than cold cardioplegia [28]. The latter findings, along with reduced postoperative cardiac troponin levels, have been replicated in other studies [29, 30]. Meanwhile, other studies comparing warm blood and cold crystalloid hyperkalemic cardioplegia do not show significant differences with respect to perioperative myocardial infarction and low cardiac output syndrome [31].
In general, administration of hyperkalemic cardioplegic solution can be done in either retrograde or anterograde fashion. Prior to both, IV heparin is administered, and the patient’s core body temperature is lowered to hypothermic levels, after which the aortic cross-clamp is placed and cardiopulmonary bypass is initiated [7]. Anterograde cardioplegia refers to delivering cardioplegic solution through a cannula inserted just proximal to the aortic cross-clamp. From there, the solution can flow into the left and right coronary arteries that supply the myocardium [32]. With anterograde cardioplegia, arrest usually occurs within 30 to 60 seconds. Retrograde cardioplegia may be considered in patients with complications such as severe coronary artery damage (e.g. severe stenosis) or aortic valve damage. Unlike anterograde administration, in retrograde administration the cardioplegia catheter is inserted into the coronary sinus from the right atrium, and solution is injected at a lower pressure (given the lower tolerance of the coronary sinus walls to turbulent flow) to avoid coronary sinus perforation [32].
Under physiological circumstances, the cardiomyocyte resting membrane potential is largely determined by two key factors: action of the sodium-potassium ATPase, and the high resting permeability of cardiomyocyte cell membranes to potassium [33]. First, the sodium-potassium ATPase hydrolyzes ATP to continuously pump potassium into the cell and sodium out of the cell, with a relative ratio of 3Na out/2 K in per molecule of ATP. Because it is the primary ion pump active while the cell is at rest, the sodium-potassium ATPase plays a critical role in generating the characteristic sodium and potassium electrochemical gradients across the cardiomyocyte cell membrane (high potassium and low sodium inside the cell relative to out). Second, at rest the cardiomyocyte cell membrane is most permeable to potassium while being relatively impermeable to other ions. This results in a resting membrane potential for cardiomyocytes that is close to the Nernst equilibrium potential for potassium, roughly −85 to -90 mV.
During cardiac muscle contraction, sinoatrial node stimulation induces a transient increase in the resting membrane potential of cardiomyocytes, which in turn opens voltage-gated sodium channels once the membrane potential surmounts -65 mV. Due to the high inward ion driving force on sodium (based on the considerable difference between the Nernst potential for sodium and the resting membrane potential), sodium ions flow through the sodium channels into the cardiomyocyte and further depolarize the cell until it reaches about 20 mV. At this point, sodium channels inactivate and L-type voltage gated calcium channels take over the maintenance of the action potential, allowing influx of calcium ions and producing the classic plateau depolarization of cardiac ventricular action potentials. Eventually, as calcium channels close and membrane potential begins to dip, delayed rectifier potassium channels open and restore membrane potential to the resting state. By this point, enough calcium has entered the cardiomyocyte to promote calcium-induced calcium release from intracellular calcium stores in the cardiomyocyte sarcoplasmic reticula, allowing muscle contraction to occur.
Extracellular hyperkalemia is the core principle underpinning most warm blood and cold crystalloid cardioplegic solutions. Essentially, administration of hyperkalemic solution takes advantage of the pivotal role of the potassium electrochemical gradient in determining cardiomyocyte resting membrane potential in order to elevate the resting membrane potential to a less negative value than typical baseline level. For example, physiologic extracellular potassium levels are often in the range of 3.5–5 mM, producing a resting membrane potential around -85 mV. During cardiac surgery involving cardioplegia, hyperkalemic solutions often raise extracellular potassium to the range of 10-40 mM (often midway in this range, around the 25 mM level), elevating cardiomyocyte resting membrane potentials to anywhere between −65 to -40 mV [34]. Arresting cardiomyocytes at this new range of elevated membrane potentials promotes fast sodium channel inactivation, thereby blocking myocardial action potential conduction. It also blocks repolarization, which is why hyperkalemic cardioplegia induces what is called “depolarized arrest.” Finally, it is important to note that cardioplegic arrest also significantly reduces cardiomyocyte oxygen consumption in a manner reminiscent of how severe ischemia depletes cellular ATP reserves [33].
Despite its clinical usefulness in reversibly arresting the heart during cardiac surgery, sustained depolarized hyperkalemic cardioplegia is not without some negative perioperative consequences. First, while most voltage-gated “fast” sodium channels are inactivated at membrane potentials above -50 mV (a frequent target cardiomyocyte membrane potential for potassium cardioplegia), resulting in generally poor membrane sodium conductance, not
Similarly, ATP depletion and reduced myocardial oxygen consumption during hyperkalemic cardioplegia leads to myocardial ischemia. Ischemia forces myocardial cells to resort to anaerobic glycolysis for energy production, which generates lactate as a byproduct. Increasing lactate levels in cardiomyocytes produces a metabolic acidosis and promotes increased activity of the H+/Na antiporter to move protons out of the cells at the expense of bringing in more sodium [36]. Finally, the combination of high extracellular potassium, intracellular acidosis, and hypothermia due to cold cardioplegic solution inhibits action of the sodium-potassium ATPase, which further facilitates the buildup of intracellular sodium [34].
Note that -50 mV is also in the vicinity of the reversal potential of the sodium/calcium exchanger [37, 38]. Under normal circumstances, the sodium/calcium exchanger moves 3 Na in for every 1 Ca moved out of the cell. However, due to the sodium window current and depolarized arrest in hyperkalemic cardioplegia, the sodium/calcium exchanger eventually begins operating in reverse, moving 3 Na out for every 1 Ca in, producing a so-called calcium “window current.” Moreover, if the hyperkalemic cardioplegic solution holds cardiomyocyte membrane potentials above -50 mV, e.g. at around -40 mV, then voltage-gated slow calcium channels will begin to activate, causing further calcium influx [39]. All of these reasons help explain why many hyperkalemic cardioplegic solutions in clinical practice are also hypocalcemic relative to physiological extracellular calcium levels (or contain calcium channel blockers), to attempt to mitigate the severity of myocardial calcium loading [34].
Cytosolic calcium loading during hyperkalemic cardioplegia contributes to cardiomyocyte damage through several mechanisms [40]. Enhanced activation of calcium dependent proteases and lipases (e.g. phospholipases) contributes to plasma membrane phospholipid degradation, ultrastructural changes in the sarcolemmal membrane, and accumulation of pathological catabolic byproducts. Enhanced activation of calcium-dependent ATPases accelerates depletion of intracellular ATP stores that have already been lowered following hypothermic arrest. This further perturbs cardiomyocyte sarcolemmal calcium transport channels that rely on ATP to maintain intracellular calcium homeostasis. Moreover, hypoxia during hyperkalemic cardioplegia increases mitochondrial calcium uptake via reversal of mitochondrial sodium/calcium exchangers in a manner akin to reversal of cardiomyocyte cell membrane sodium/calcium exchangers [41].
Mitochondria can only endure so much calcium uptake before the onset of irreversible damage. Indeed, following reperfusion after hyperkalemic cardioplegia arrest, mitochondria exhibit increased oxygen free radical production and reduced superoxide dismutase activity, indicative of heightened oxidative stress [41]. Sustained oxidative stress can lead to opening of mitochondrial permeability transition pores (MPTP), which promote mitochondrial swelling and mitochondrial membrane rupture. An assortment of mitochondrial enyzmes and molecules, such as cytochrome c, leak out into the cytosol through the MPTPs [41]. Cytochrome c is implicated in intrinsic apoptotic pathways through activation of cytosolic caspases and subsequent formation of myocardial apoptosomes [41].
Myocardial apoptosis during hyperkalemic cardioplegic ischemia–reperfusion merits further consideration for two major reasons. First, several studies have shown associations between hyperkalemic cardioplegic arrest and endothelial cell and cardiomyocyte apoptosis [42, 43, 44]. Second, several independent pathways of myocardial cell injury converge on apoptosis. Examples include mitochondrial oxidative stress and activation of an intrinsic apoptotic pathway (introduced earlier), or an extrinsic pathway driven by elevated humoral factors such as Fas or TNF-alpha acting on pro-apoptosis cell membrane receptors [44, 45]. Both intrinsic and extrinsic pathways converge upon a similar final common pathway that is chiefly regulated by two key protein groups: the Bcl-2 and cysteine protease caspase families [46, 47].
Within the Bcl-2 family, two proteins are particularly significant: Bcl-2 itself, and Bad. The former is anti-apoptotic while the latter is pro-apoptotic. Phosphorylation inhibits Bad, blocking it from inactivating Bcl-2 [48]. Farther downstream in apoptotic signaling, cleavage of caspase 3 and poly ADP-ribose polymerase (PARP) is essential for ensuring final progression towards apoptosis. Meanwhile, apoptosis may also proceed via a caspase-independent pathway involving release of the mitochondrial flavoprotein apoptosis-inducing factor (AIF) from the mitochondria into the cytosol through MPTPs [49, 50].
A possible framework for understanding myocardial apoptosis after hyperkalemic CPB is as follows [48]. Activation of the intrinsic (mitochondrial) pathway leads to increased Bad activation/decreased Bcl-2 activation, which initiates the caspase cascade. Activation of the extrinsic pathway bypasses Bcl-2/Bad to directly activate the caspase cascade. As more and more caspases become activated, eventually terminal caspases, such as caspase 3, will be cleaved, leading to PARP cleavage. By this point, apoptosis has been irreversibly induced; DNA fragmentation and cell death quickly follow. In contrast, AIF translocation from the mitochondria to the cytosol may directly activate downstream/terminal caspases, bypassing initial/intermediary constituents of the caspase cascade.
Studies have shown that caspase 3 cleavage and Bcl-2/Bad phosphorylation are significantly increased in myocardial tissue following hyperkalemic cold-blood cardioplegia and reperfusion, even as total protein levels do not change [48]. Meanwhile, myocardial AIF levels increase slightly, accompanied by a trend towards nuclear translocation, consistent with a model of AIF induced chromatin condensation and DNA fragmentation as a mechanism of cell injury [48]. Note that both pro-apoptotic (e.g. caspase 3) and anti-apoptotic (e.g. phosphorylated Bad) mediators are activated—nevertheless, given the downstream terminal position of caspase 3, the overall balance in myocardial cells appears to be tipped in favor of pro-apoptotic signaling.
Different formulations of hyperkalemic cardioplegia (e.g. cold crystalloid, warm blood, etc.) may exhibit differing degrees of myocardial protection and prevention of apoptosis. Indeed, evidence exists suggesting that cold blood hyperkalemic cardioplegia is superior to warm blood, warm crystalloid, and cold crystalloid cardioplegia, in terms of increased Bad phosphorylation and decreased caspase 3 activation [51]. Taken together, this combination of events appears to result in less apoptosis. In addition, these effects are associated with improved left ventricular function following cardioplegic arrest. However, this is not a universal finding in the literature. More work must be done to verify these conclusions and confirm if there truly is a definitive benefit to any one technique of hyperkalemic cardioplegia with respect to prevention of apoptosis.
An extensive body of research has established that hyperkalemic solutions induce significant vasoconstriction when experimentally applied to coronary artery and aortic ring preparations [2]. Thus, it is no surprise that hyperkalemic cardioplegia induces significant functional changes to the microcirculation, especially the coronary circulation [52]. For example, a sizeable number of patients undergoing hyperkalemic cardioplegia experience coronary artery spasm [52].
Potassium can influence coronary vasoconstriction in several ways. Holding coronary vascular smooth muscle membrane potentials at sustained depolarization during hyperkalemic cardioplegia increases the likelihood of generating contractions [53]. Potassium may also act indirectly to cause vasospasm through action on the coronary endothelium. Indeed, endothelial vasoconstrictive and vasorelaxant factors govern homeostatic regulation of coronary vasomotor tone. These factors influence vascular smooth muscle through modulation of various cell membrane potassium channels, including calcium-activated potassium channels and ATP-activated potassium channels [54, 55]. Important endothelial-derived relaxing factors include nitric oxide, endothelial-derived hyperpolarizing factor (EDHF), and cyclooxygenase enzymes. Important endothelial-derived constricting factors include endothelin-1 and thromboxane A2.
Porcine models of hyperkalemic cardioplegia showed that hyperkalemia significantly attenuated EDHF-mediated relaxation in coronary artery preparations [56, 57]. Moreover, hyperkalemic vasoconstriction has also been linked with impaired nitric oxide release [58] and impaired acetylcholine-dependent vascular relaxation [59, 60]. Potential mechanisms at play may involve potassium-induced inhibition of G protein and non-G protein signal transduction pathways, increased reactive oxygen and nitrogen species generation, decreased activity of endothelial nitric oxide synthase, and increased arachidonic acid metabolism [2]. Curiously, hyperkalemic cardioplegia has also been associated with decreased responsiveness of human coronary arterioles to the endothelial vasoconstrictors endothelin-1 and thromboxane A2 [61, 62]. These findings testify to the complexity of mechanisms underpinning coronary vasomotor dysfunction following hyperkalemic cardioplegia, most of which remain to be elaborated.
Despite its cardioprotective effects, hyperkalemic cardioplegia-reperfusion can exert detrimental effects on the myocardial and coronary endothelium, promoting endothelial dysfunction [63, 64]. One aspect of endothelial dysfunction—production of various endothelium-derived relaxing and contracting factors—was discussed earlier due to its relevance in coronary vasospasm. Other important features of endothelial dysfunction during hyperkalemic cardioplegic arrest include endothelial injury, inflammation, reactive oxygen species production, coagulation cascade dysfunction, and endothelial tight junction degradation [52, 65, 66, 67]. All these adverse effects may occur with potassium levels as low as 10 mM, well within the realm of most hyperkalemic cardioplegic solutions [2]. To elaborate, potassium concentrations of 30 mM in St. Thomas and Custodiol cardioplegic solutions proved considerably more damaging to the vascular endothelium than potassium concentrations of 20 mM, demonstrating the importance of strict potassium limits in hyperkalemic cardioplegic solutions [6].
A variety of structural changes to the vascular endothelium have been observed in experimental models of hyperkalemic cardioplegia. Key examples include endothelial intracellular vacuolization, membrane blebbing, adventitial fibrosis, and overall reduced viability [68, 69]. Furthermore, hyperkalemic cardioplegia promotes increased lipid uptake and cholesterol deposition in vascular intimae in primate models of post-graft venous atherosclerosis [70]. In addition, compromised endothelial adherens junctions during hyperkalemic cardioplegia mediate increased vascular permeability and tissue edema [67]. Indeed, animal models of cardioplegia/CPB show increased post-procedure VE cadherin, beta-catenin, and gamma-catenin fragments, all of which are important structural components of adherens junctions [71]. In humans, increased endothelial cadherin phosphorylation, and decreased overall beta-catenin levels, have been observed in atrial tissue following hyperkalemic cardioplegia/CPB [72].
Details of specific mechanisms underlying these endothelial disturbances remain largely unclear; however, many possibilities exist. For example, it is generally agreed that depolarization induced by hyperkalemic cardioplegia is a critical initiating step of the underlying pathophysiology [2]. Endothelial depolarization increases activation of neutrophils, inflammation, voltage sensitive NAPDH oxidases, and platelets [62, 63, 73, 74]. Inflammation and neutrophil activation often reinforce each other, as pro-inflammatory cytokines like IL-1, IL-6, and TNF-alpha further stimulate endothelial changes that promote neutrophil extravasation. NADPH oxidase catalyzes formation of important reactive oxygen species such as superoxide anions, which if left unchecked are severely cytotoxic. The amount of superoxide production during hyperkalemic cardioplegia has been linked to the extent of endothelial depolarization and translocation of the small G protein Rac from the cytosol to plasma membrane [75].
With respect to coagulation, potassium depolarization appears to have a direct stimulatory effect via enhancing ADP and collagen-induced platelet aggregation, along with an indirect effect through increased superoxide production [76, 77]. The latter appears to act through inhibition of endothelial NTPDases [78]. Membrane hyperpolarization reverses all these actions.
When left unchecked, sustained myocardial dysfunction following hyperkalemic cardioplegia-reperfusion may lead to myocardial stunning, a form of postoperative left ventricular dysfunction [1]. Myocardial stunning often manifests as markedly reduced cardiac output without obvious evidence of infarction or injury (e.g. no signs of elevated troponin or CKMB in blood). Like myocardial apoptosis, myocardial stunning represents another final common pathway of convergence for several different pathophysiological mechanisms of hyperkalemic cardioplegia, chiefly dysregulated free radical production, coagulation imbalances, and excessive catecholamine release [1]. However, unlike with apoptosis, in this scenario injury results from abnormal myocardial contractility as opposed to myocardial cell death.
Postoperative imbalances in a variety of different electrolytes, including calcium, magnesium, potassium, and phosphate, have been observed following cardioplegia/CPB. Here, we will focus on potassium, beginning with hypokalemia. Hypokalemia can be defined as a serum potassium level that is less than 3.5 mEq/L [78]. Postoperative hypokalemia is a common finding after cardiac surgery involving hyperkalemic cardioplegia and CPB, and manifests almost immediately after the patient is weaned off the bypass circuitry [79]. Hence IV potassium supplementation during cardioplegia is extremely important to mitigate against the most severe manifestations [80].
However, even with electrolyte supplementation in the operating room, CPB poses a high risk of post-procedure electrolyte depletion [81]. The pivotal role of potassium in normal cardiac contractility means that disturbances in potassium homeostasis significantly increase the risk of arrythmias and, in severe cases, sudden cardiac arrest. Indeed, arrythmias, especially atrial tachyarrhythmias (e.g. atrial fibrillation, atrial flutter) and, less frequently, ventricular arrhythmias, are a major source of morbidity and mortality following cardiac surgery [82, 83].
Specific mechanisms underpinning this phenomenon remain largely unclear; however, a variety of possibilities exist [78]. For example, poor oral intake of potassium-rich foods prior to cardiac surgery may contribute to enhanced depletion during surgery. In addition, prolonged preoperative use of digoxin, along with thiazide and loop diuretics may play a role. These agents may cause hypomagnesemia (low magnesium levels), which can contribute to extracellular potassium depletion. Under normal circumstances, intracellular magnesium binds to and blocks the pores of renal outer medullary potassium (ROMK) channels in the distal nephron, preventing outward flux of potassium into the renal tubular network [78]. Thus hypomagnesemia may remove this physiologic limiter, leading to increased renal clearance of potassium.
A hyperactive aldosterone response to stress may also be implicated, particularly in the context of congestive heart failure [78, 80]. Moreover, increased catecholamine (norepinephrine and epinephrine) release during cardiopulmonary bypass may facilitate hypokalemia given the influence of catecholamines on plasma potassium [84, 85]. Animal models have shown that elevated catecholamine levels can produce first, a transient hyperkalemia due to activation of hepatic calcium-dependent potassium channels by alpha adrenergic stimulation and second, a sustained hypokalemia by stimulation of skeletal muscle Na-K ATPase [86]. Such studies need to be replicated in humans undergoing cardiopulmonary bypass-hyperkalemic cardioplegia in order to verify the applicability of these putative mechanisms.
Because glucose is often given during cardioplegia, insulin may also be administered to minimize the chances of hyperglycemia. However, given that insulin acts as a regulator of potassium distribution between intracellular and extracellular fluid compartments by stimulating Na-K ATPase activity, it is possible that insulin administration during and after cardioplegia may contribute to potassium depletion [87]. Next, given that many cardioplegic solutions in current practice are cold hyperkalemic solutions, any potential impact of hypothermia on potassium homeostasis during cardiac surgery cannot be ignored. As with insulin, hypothermia has been linked to an intracellular shift of potassium away from the extracellular space through as-yet unelaborated mechanisms [88]. Finally, the CPB circuit itself has been shown to significantly dilute overall blood plasma protein concentrations, which may also affect plasma ion homeostasis [89].
In general, treatment of postoperative hypokalemia largely centers on administration of potassium chloride (KCl) solution to elevate extracellular potassium concentrations to physiologic levels. Indeed, in the case of pediatric cardiac ICU patients for whom enteral potassium supplementation is contraindicated, IV KCl administration is one of the only available tools for correcting hypokalemia [90]. For most patients, this proves sufficient to correct the imbalance and stave off the development of hypokalemia-induced arrhythmias. However, in a small minority, external KCl solution does not reverse the hypokalemia—and so in these patients, the chances of arrhythmias increase exponentially.
Although hypokalemia is the most common potassium electrolyte abnormality following hyperkalemic cardioplegia-CPB, postoperative hyperkalemia may occur under certain, albeit rarer, circumstances. In general, postoperative hyperkalemia is a concern mainly in patients with renal failure undergoing CPB, most likely due to renal tubular dysfunction [91]. Severe hyperkalemia may be treated with IV calcium gluconate, an insulin-dextrose regimen, and diuretics [92]. If a patient has end-stage renal disease, dialysis may be the best option to treat hyperkalemia, along with IV calcium to stabilize the myocardium and IV insulin to shift potassium into cells [93].
Hyperkalemic cardioplegia is by far the most widely used method of cardioplegia in current clinical practice. However, because of the numerous perioperative repercussions of hyperkalemic cardioplegia, a variety of attempts have been made to explore alternative approaches. Given that many adverse effects of hyperkalemic cardioplegia stem from its induction of depolarized arrest, one popular avenue of investigation has been the possibility of hyperpolarized arrest. Hyperpolarization is the natural resting state of cardiomyocytes, so in theory, arresting the heart at its baseline hyperpolarized state may better preserve physiological integrity. In isolated animal heart models, hyperpolarized arrest has been achieved via pharmacologic activation of ATP-sensitive potassium channels [94, 95]. Following reperfusion, this form of hyperpolarized arrest appeared to lead to improved postischemic functional recovery when compared to hearts protected with depolarized arrest.
Meanwhile, so-called “polarized arrest” has been proposed as another alternative to hyperkalemic cardioplegia. The core principle behind this concept is administration of sodium channel blockers, such as procaine in humans or tetrodotoxin in animal models [96]. Sodium channel blockade prevents depolarization-induced activation of calcium currents, which normally carry out the bulk of the cardiomyocyte action potential. Overall, in animal models, tetrodotoxin-induced polarized arrest reduces metabolic demands during ischemia, including myocardial oxygen consumption, more so than hyperkalemic cardioplegia [96]. Furthermore, polarized arrest may produce less significant postoperative ionic imbalances, with further protection provided by coincident administration of sodium/potassium/chloride transporter and sodium/proton exchanger inhibitors [96]. Nonetheless, more work needs to be done to verify the broader clinical applicability of these alternatives to hyperkalemic cardioplegia.
By taking advantage of the pivotal role of potassium in cardiomyocyte physiology, hyperkalemic cardioplegia has become an integral tool for cardiac surgery. From the early days of Dennis Melrose’s simple potassium citrate solution to complex modern-day formulations such as the Del Nido and Buckberg media, approaches to developing and administering hyperkalemic cardioplegic solutions have evolved considerably, with a continuing focus on developing the most cardioprotective and least damaging solutions possible. While initial approaches to hyperkalemic cardioplegia revolved around hypothermic solutions, normothermic/“warm” solutions, along with blood as opposed to crystalloid-based solutions, are gaining momentum as potential alternatives to mitigate adverse perioperative consequences of cold hyperkalemic cardioplegia. Some of those consequences include myocardial calcium loading, myocardial apoptosis, coronary vasomotor dysfunction, myocardial endothelial dysfunction, and myocardial stunning. With any form of hyperkalemic cardioplegia, plasma potassium abnormalities following reperfusion, mainly postoperative hypokalemia, remain a persistent clinical concern. And while most patients respond well to IV KCl supplementation, some do not and proceed to develop fatal arrythmias, underscoring the need for further research to understand the mechanisms at play and develop new treatments. In the future, it is possible that other approaches such as hyperpolarized or polarized arrest may challenge the widespread use of depolarized hyperkalemic cardioplegic arrest. Nevertheless, for the time being, hyperkalemic cardioplegia remains dominant in cardiac surgery, and will likely continue to be so for some time to come.
The authors have no acknowledgements.
The authors declare no conflicts of interest.
The authors have no other notes or declarations.
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Wireless power transmission (WPT) technology was first pursued by Tesla over a century ago. However, it faced several challenges for deployment in real applications. Recently, energy harvesting and WPT technologies have received much attention as a clean and renewable power source. Rectenna (rectifying antenna) system can be used for remotely charging batteries in several sensor networks at internet of things (IoT) applications as commonly used in smart buildings, implanted medical devices and automotive applications. Rectenna, which is used to convert from RF energy to usable DC electrical energy, is mainly a combination between a receiving antenna and a rectifier circuit. This chapter will present several designs for single and multiband rectennas with different characteristics for energy harvesting applications. Single and multiband antennas as well as rectifier circuits with matching networks are introduced for complete successful rectenna circuit models. 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Further, the improved dual circularly polarized (CP) omnidirectional antenna based on slot array in coaxial cylinder structure is presented too, and two ports are assigned in its two side as left hand circularly polarized (LHCP) port and right hand circularly polarized (RHCP) port, respectively. The simulation and experiment results show their novelty and good performance of omnidirectional circular polarization with about 5 dBi gain in 5.2–5.9 GHz.",book:{id:"5427",slug:"modern-antenna-systems",title:"Modern Antenna Systems",fullTitle:"Modern Antenna Systems"},signatures:"Bin Zhou, Junping Geng, Xianling Liang, Ronghong Jin and\nGuanshen Chenhu",authors:[{id:"147056",title:"Prof.",name:"Xian-Ling",middleName:null,surname:"Liang",slug:"xian-ling-liang",fullName:"Xian-Ling Liang"},{id:"189327",title:"Prof.",name:"Junping",middleName:null,surname:"Geng",slug:"junping-geng",fullName:"Junping Geng"},{id:"189923",title:"Prof.",name:"Ronghong",middleName:null,surname:"Jin",slug:"ronghong-jin",fullName:"Ronghong Jin"},{id:"189925",title:"MSc.",name:"Bin",middleName:null,surname:"Zhou",slug:"bin-zhou",fullName:"Bin Zhou"},{id:"189927",title:"MSc.",name:"Guanshen",middleName:null,surname:"Chenhu",slug:"guanshen-chenhu",fullName:"Guanshen Chenhu"}]}],onlineFirstChaptersFilter:{topicId:"762",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:0,limit:8,total:null},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:87,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:98,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:27,numberOfPublishedChapters:287,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:9,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:139,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:0,numberOfUpcomingTopics:2,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!1},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:107,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:10,numberOfPublishedChapters:103,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:12,numberOfOpenTopics:2,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:0,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!1},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:10,numberOfOpenTopics:4,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. 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He completed a one-year Post-Doctoral Fellowship awarded by the DFAIT (Foreign Affairs and International Trade Canada) at the Institute of Biomedical Engineering of the University of New Brunswick (Canada) in 2010. Currently, he is Professor in the Faculty of Electrical Engineering (UFU). He has authored and co-authored more than 200 peer-reviewed publications in Biomedical Engineering. He has been a researcher of The National Council for Scientific and Technological Development (CNPq-Brazil) since 2009. He has served as an ad-hoc consultant for CNPq, CAPES (Coordination for the Improvement of Higher Education Personnel), FINEP (Brazilian Innovation Agency), and other funding bodies on several occasions. He was the Secretary of the Brazilian Society of Biomedical Engineering (SBEB) from 2015 to 2016, President of SBEB (2017-2018) and Vice-President of SBEB (2019-2020). 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He is an author and co-author of scientific publications covering analysis and processing of biomedical images and development of database systems.",institutionString:"University of Silesia",institution:null}]},{type:"book",id:"6843",title:"Biomechanics",subtitle:null,coverURL:"https://cdn.intechopen.com/books/images_new/6843.jpg",slug:"biomechanics",publishedDate:"January 30th 2019",editedByType:"Edited by",bookSignature:"Hadi Mohammadi",hash:"85132976010be1d7f3dbd88662b785e5",volumeInSeries:4,fullTitle:"Biomechanics",editors:[{id:"212432",title:"Prof.",name:"Hadi",middleName:null,surname:"Mohammadi",slug:"hadi-mohammadi",fullName:"Hadi Mohammadi",profilePictureURL:"https://mts.intechopen.com/storage/users/212432/images/system/212432.jpeg",biography:"Dr. Hadi Mohammadi is a biomedical engineer with hands-on experience in the design and development of many engineering structures and medical devices through various projects that he has been involved in over the past twenty years. Dr. Mohammadi received his BSc. and MSc. degrees in Mechanical Engineering from Sharif University of Technology, Tehran, Iran, and his PhD. degree in Biomedical Engineering (biomaterials) from the University of Western Ontario. He was a postdoctoral trainee for almost four years at University of Calgary and Harvard Medical School. He is an industry innovator having created the technology to produce lifelike synthetic platforms that can be used for the simulation of almost all cardiovascular reconstructive surgeries. He’s been heavily involved in the design and development of cardiovascular devices and technology for the past 10 years. 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