Natural cardiotoxic toxins from plants: source, structure, receptors, mode of action, effects on heart and toxicity.
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",isbn:"978-1-83962-547-3",printIsbn:"978-1-83962-546-6",pdfIsbn:"978-1-83962-548-0",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,hash:"e5ba02fedd7c87f0ab66414f3b07de0c",bookSignature:"Dr. John P. Tiefenbacher",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10765.jpg",keywords:"Managing Urbanization, Managing Development, Managing Resource Use, Drought Management, Flood Management, Water Quality Monitoring, Air Quality Monitoring, Ecological Monitoring, Modeling Extreme Natural Events, Ecological Restoration, Restoring Environmental Flows, Environmental Management Perspectives",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"January 12th 2021",dateEndSecondStepPublish:"February 9th 2021",dateEndThirdStepPublish:"April 10th 2021",dateEndFourthStepPublish:"June 29th 2021",dateEndFifthStepPublish:"August 28th 2021",remainingDaysToSecondStep:"a month",secondStepPassed:!0,currentStepOfPublishingProcess:3,editedByType:null,kuFlag:!1,biosketch:"A geospatial scholar working at the interface of natural and human systems, collaborating internationally on innovative studies about hazards and environmental challenges. Dr. Tiefenbacher has published more than 200 papers on a diverse array of topics that examine perception and behaviors with regards to the application of pesticides, releases of toxic chemicals, environments of the U.S.-Mexico borderlands, wildlife hazards, and the geography of wine.",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"73876",title:"Dr.",name:"John P.",middleName:null,surname:"Tiefenbacher",slug:"john-p.-tiefenbacher",fullName:"John P. Tiefenbacher",profilePictureURL:"https://mts.intechopen.com/storage/users/73876/images/system/73876.jfif",biography:"Dr. John P. Tiefenbacher (Ph.D., Rutgers, 1992) is a professor of Geography at Texas State University. His research has focused on various aspects of hazards and environmental management. Dr. Tiefenbacher has published on a diverse array of topics that examine perception and behaviors with regards to the application of pesticides, releases of toxic chemicals, environments of the U.S.-Mexico borderlands, wildlife hazards, and the geography of wine. More recently his work pertains to spatial adaptation to climate change, spatial responses in wine growing regions to climate change, the geographies of viticulture and wine, artificial intelligence and machine learning to predict patterns of natural processes and hazards, historical ethnic enclaves in American cities and regions, and environmental adaptations of 19th century European immigrants to North America's landscapes.",institutionString:"Texas State University",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"6",institution:{name:"Texas State University",institutionURL:null,country:{name:"United States of America"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"12",title:"Environmental Sciences",slug:"environmental-sciences"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"194667",firstName:"Marijana",lastName:"Francetic",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/194667/images/4752_n.jpg",email:"marijana@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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Several natural toxins are produced by plants, bacteria, phytoplanktonic dinoflagellates, sea anemones, insects, fungi and animals. In nature, toxins have two main functions: to capture their preferred prey (e.g. spiders, snakes, scorpions, etc.) or to serve as defence (e.g. bee sting, frog poison, etc.). Toxins produced by micro-organisms are important virulence factors. On the other hand they are also tools to combat diseases. Some of them are used in low quantities as drugs, to prepare vaccines and as important tools in biomedical research. Toxins affecting heart physiology are very effective in the sense of defence and especially in capturing prey. They can disturb electrical (producing arrhythmias) and mechanical activity of the heart affecting pumping or leading even to cardiac arrest. The aim of this chapter is to describe most of the toxins affecting heart function, their targets in the heart tissue, mode of action and the most important clinical effects of envenomation.
\n\t\tVoltage-gated sodium channels are an essential part of excitable membranes and enable fast depolarisation, which is responsible for action potential (AP) generation in cardiomyocytes and in the some parts of the conduction system of the heart. Their density is very low in some parts of the heart\'s conductive system, e.g. sinoatrial node and atrioventricular node cells, and the highest in Purkinje cells and cardiomyocytes (Fozzard, 1996). Hence, they are targeted by several neurotoxins from plants and animals that use these molecules for defence and protection.
\n\t\t\tDifferent types of Ca2+-permeable channels have been described in the plasma membrane of heart cells: the L- and T-type channels, both voltage activated, and a background channel (for a review see Carmeliet et al., 1999). Inward current through L-type high voltage-gated calcium channels is responsible for prolonged AP in cardiac muscle cells and cardiac muscle contraction. L-type voltage-gated Ca2+-channels are especially target for some bacterial (saxitoxin) and animal toxins (atrotoxin, maitotoxin, -conotoxin, crotoxin).
\n\t\t\tThe role of potassium channels is to repolarize the membrane during the AP or to maintain hyperpolarizing potential. They are involved in the regulation of duration of the AP. Therefore, changes in the function of potassium channels may cause life-threatening arrhythmias (Carmeliet et al., 1999). Important potassium channels that can be the target of natural toxins are calcium-activated potassium channels (charybdotoxin, iberiotoxin, apamin) and voltage-gated potassium channels (some dendrotoxins).
\n\t\t\tAconitines are a group of very poisonous alkaloids derived from various aconite species. They are neurotoxins that open TTX-sensitive Na+ channels in the heart and other tissues (Wang & Wang, 2003). Some of them can bind to the high affinity receptor site 2 of sodium channels (Ki ~1.2 µM) and some of them to a low affinity binding site (Ki ~11.5 µM). The compounds of the high affinity group, which increases synaptosomal sodium and calcium activity (EC50 3 µM), are the most toxic and provoke tachyarrhythmia. Binding of aconitine to the site II of voltage-dependent Na+ channels prolongs the open state responsible for Na+ influx leading to the permanent depolarization. Now it is commonly accepted that aconitine produces arrhythmias by prolonging opening or delaying the inactivation of voltage-dependent Na+ channels. Low affinity alkaloids from aconitum species are less-toxic, reduce intracellular calcium activity and induce bradycardia (Friese et al., 1997).
\n\t\t\t\tAt least four grayanotoxins (GTXs) have been isolated from the leaves of Rhododendron decorum (Ericaceae). These toxins are responsible for so called "mad honey" intoxication. Early in the 1980s it was published that GTXs produce cardiac tachyarrhythmias. The pathophysiological mechanism, underlying tachyarrhythmia, is the triggered activity in the form of oscillatory afterpotentials, as it was shown in feline cardiac Purkinje fibres (Brown et al., 1981). After intoxication, GTXs can produce bradyarrhythmias in man and livestock (Koca & Koca, 2007). It was shown that GTXs-induced cardiac toxicity in rats is a consequence of increased sodium channel permeability and activated vagus nerve (Onat et al., 1991). Intoxication is associated with the fatal bradyarrhythmias that include second degree atrio-ventricular block and circulatory collapse (Okuyan et al., 2010).
\n\t\t\t\tVeratrum species plants contain more than 200 different alkaloids, which are the principal toxins. The opening of voltage-gated sodium channels is probably one of the most relevant pathophysiological mechanisms of its toxicity. Veratridine injected intravenously in rats induced the Bezold-Jarisch-like effect (transient hypotension) accompanied by bradicardia (Chianca et al., 1985). It is well known that persistent sodium current, which can be enhanced during heart ischemia, is one of the major contributors to ischemic arrhythmias. Prolonged cardiac AP, which can also be induced by veratridine, favours the occurrence of early afterdepolarizations that is one of the pathophysiological mechanisms of tachyarrhythmias. Increased Na+ uptake activates the Na+/Ca2+ exchanger that leads to cardomyocytes’ Ca2+ overload. The latter can trigger the late depolarization after-potentials (DAPs), which is another pathophysiological mechanism underlying arrhythmias. If the amplitude of the DAPs reaches the threshold potential, a new AP is triggered. Such large, late DAPs often occur in the case of oscillations of the cytosolic Ca2+ concentration (Pignier et al., 2010).
\n\t\t\t\t\tName | \n\t\t\t\t\t\t\t\tSource (produced by) | \n\t\t\t\t\t\t\t\tChemical structure | \n\t\t\t\t\t\t\t\tTarget | \n\t\t\t\t\t\t\t\tMode of action | \n\t\t\t\t\t\t\t\tEffects | \n\t\t\t\t\t\t\t\tAcute LD50 in mice | \n\t\t\t\t\t\t\t\tReference | \n\t\t\t\t\t\t\t
Cardiotoxic toxins from plants | \n\t\t\t\t\t\t\t|||||||
Aconitine | \n\t\t\t\t\t\t\t\tPlants from genus Aconitum | \n\t\t\t\t\t\t\t\tAlkaloid | \n\t\t\t\t\t\t\t\tVoltage-gated Na+ channels | \n\t\t\t\t\t\t\t\tDepolariza-tion, AP duration increase | \n\t\t\t\t\t\t\t\tArrhy-thmias | \n\t\t\t\t\t\t\t\t0.1 mg/kg | \n\t\t\t\t\t\t\t\tGutser, 1998 | \n\t\t\t\t\t\t\t
Grayanoto-xins (GTX) | \n\t\t\t\t\t\t\t\tSpecies from genus Rhododendron | \n\t\t\t\t\t\t\t\tPolyhydro-xylated cyclic diterpene | \n\t\t\t\t\t\t\t\tIncrease Na+ channel permeability and activate vagus nerve | \n\t\t\t\t\t\t\t\tAlteration of excitability | \n\t\t\t\t\t\t\t\tFatal cardiac bradyar-rhythmias | \n\t\t\t\t\t\t\t\t1.28 mg/kg i.p. | \n\t\t\t\t\t\t\t\tBrown et al., 1981; Okuyan et al., 2010 ; Scott et al., 1971 | \n\t\t\t\t\t\t\t
Veratridine | \n\t\t\t\t\t\t\t\tPlants in the family Liliaceae | \n\t\t\t\t\t\t\t\tSteroid-derived alkaloid | \n\t\t\t\t\t\t\t\tBinding to the activated Na+ ion channels | \n\t\t\t\t\t\t\t\tDepolariza-tion, AP duration increase | \n\t\t\t\t\t\t\t\tArrhy-thmias | \n\t\t\t\t\t\t\t\t1.35 mg/kg i.p. | \n\t\t\t\t\t\t\t\tChianca et al., 1985; Pignier et al., 2010; Swiss & Bauer, 1951 | \n\t\t\t\t\t\t\t
Natural cardiotoxic toxins from plants: source, structure, receptors, mode of action, effects on heart and toxicity.
Ostreolysin (Oly) is an acidic, 15 kDa protein isolated from the edible oyster mushroom (Pleurotus ostreatus) (Berne et al., 2002). It is a toxic, pore-forming cytolysin (Sepčić et al., 2003). When administered intravenously (i.v.), Oly causes electrocardiographic, arterial blood pressure and respiratory changes. Oly produces changes such as transient increase of arterial blood pressure followed by a progressive fall to mid-circulatory pressure accompanied by bradicardia, myocardial ischaemia and ventricular extrasystoles. Oly also induces lysis of rat erythrocytes in vitro and in vivo, resulting in hyperkalemia. Although direct action of the protein on the cardiomyocytes or heart circulation cannot be excluded (Oly is pore-forming toxin), the hyperkalemia resulting from the haemolytic activity seems to play an important role in its cardiotoxicity (Žužek et al., 2006). Additionally, an important mechanism of the cardiotoxic effect may also be its concentration-dependent contractile effect on elastic blood vessels, such as aorta (Rebolj et al., 2009) and coronary vessels (Juntes et al., 2009).
\n\t\t\t\t\tName | \n\t\t\t\t\t\t\t\tSource (produced by) | \n\t\t\t\t\t\t\t\tChemical structure | \n\t\t\t\t\t\t\t\tTarget | \n\t\t\t\t\t\t\t\tMode of action | \n\t\t\t\t\t\t\t\tEffects | \n\t\t\t\t\t\t\t\tAcute LD50 in mice | \n\t\t\t\t\t\t\t\tRefer-ence | \n\t\t\t\t\t\t\t
Cardiotoxic toxins derived from mushrooms | \n\t\t\t\t\t\t\t|||||||
Ostreolysin | \n\t\t\t\t\t\t\t\tOyster mushroom (Pleurotus ostreatus) | \n\t\t\t\t\t\t\t\tPore-forming protein | \n\t\t\t\t\t\t\t\tCell membranes | \n\t\t\t\t\t\t\t\tPore formation | \n\t\t\t\t\t\t\t\tBradycardia; myocardial ischaemia; ventricular extrasystoles, hyperkalemia | \n\t\t\t\t\t\t\t\t1.17 mg/kg | \n\t\t\t\t\t\t\t\tŽužek et al., 2006 | \n\t\t\t\t\t\t\t
Natural cardiotoxic toxins from mushrooms: source, structure, receptors, mode of action, effects on heart and toxicity.
\n\t\t\t\t\t\t\tVibrio parahemolyticus toxin is lethal for rats when injected i.v. in a dose of 5 g/kg or higher. It decreases intra-atrial and ventricular conductivity, and produces atrioventricular block. Before cardiac arrest occurs, ventricular flutter develops. The toxin is also toxic for cardiomyocytes in culture. Similar to the heart, the beating rhythm of cardiomyocytes exposed to the toxin increases and then abruptly stops (Honda et al., 1976).
\n\t\t\t\t\tStreptolisin O is a pore-forming toxin released in the extracellular medium by the majority of group A and some of group C and G Streptococci. It belongs to the sulphydryl- or thiol-activated toxins. It is a protein with a molecular weight of about 67 kDa. Streprolysin O is capable of forming cation permeable pores in cholesterol-rich membranes. Administered i.v. in high doses it produces sudden cardiac arrest, probably due to a non-specific binding to the lipid bilayers of cardiac cells (for a review see Harvey, 1990).
\n\t\t\t\t\tSaxitoxin (STX) is produced by certain marine species of dinoflagellates (Alexandrium sp., Gymnodinium sp.) and cyanobacteria species (Anabaena sp., some Aphanizomenon spp., Cylindrospermopsis sp.). STX, usually administered through shellfish ingestion, is responsible for the human illness known as paralytic shellfish poisoning (PSP). STX acts primarily as a sodium channel blocker; it binds to the binding site 1 (Mebs & Hucho, 1990). Additionally it was found that STX also inhibits L-type Ca2+ currents in adult mouse ventricular myocytes (Su et al., 2003).
\n\t\t\t\t\tTetrodotoxin (TTX) is a toxin of microbial origin. A number of marine bacteria probably produce TTX, especially members of the genus Vibrio (most common species is Vibrio alginolyticus). The link between this species and production of TTX in animals has not been definitely confirmed as it is not clear whether the source of TTX in animals is the above-mentioned bacteria. TTX has been isolated from many animal species (pufferfish, toads of the genus Atelopus, octopuses of the genus Hapalochlaena, etc. (Mebs & Hucho, 1990). It was shown that both high and low affinity receptors (sodium channels) for TTX exist on the rat cardiomyocytes. Only a low affinity binding site is functional on the cardiac cells, which has dissociation constant for TTX about three orders of magnitude higher compared to the reported dissociation constant for TTX receptors in muscle and nerve. The concentration needed to block cardiac sodium channels is very high (Renaud et al., 1983). The myocytes in the heart express fast voltage-gated sodium channel and therefore the generation of AP and
\n\t\t\t\t\t\tName | \n\t\t\t\t\t\t\t\t\tSource (produced by) | \n\t\t\t\t\t\t\t\t\tChemical structure | \n\t\t\t\t\t\t\t\t\tTarget | \n\t\t\t\t\t\t\t\t\tMode of action | \n\t\t\t\t\t\t\t\t\tEffects | \n\t\t\t\t\t\t\t\t\tAcute LD50 in mice | \n\t\t\t\t\t\t\t\t\tReference | \n\t\t\t\t\t\t\t\t
Microbial toxins | \n\t\t\t\t\t\t\t\t|||||||
Bacterial toxins | \n\t\t\t\t\t\t\t\t|||||||
Hemolysin TDH, TRH | \n\t\t\t\t\t\t\t\t\tVibrio parahaemolyticus | \n\t\t\t\t\t\t\t\t\tProtein | \n\t\t\t\t\t\t\t\t\tHeart | \n\t\t\t\t\t\t\t\t\tAlteration in conductance of the conductive system | \n\t\t\t\t\t\t\t\t\tArrhy-thmias, cardiac arrest | \n\t\t\t\t\t\t\t\t\tBetween 2.5 and 5 g/kg in rats | \n\t\t\t\t\t\t\t\t\tHonda et al., 1976 | \n\t\t\t\t\t\t\t\t
Streptolysin O | \n\t\t\t\t\t\t\t\t\tStreptococci group A, C and G | \n\t\t\t\t\t\t\t\t\tProtein | \n\t\t\t\t\t\t\t\t\tNonspecific binding (membranes rich on cholesterol) | \n\t\t\t\t\t\t\t\t\tPore formation | \n\t\t\t\t\t\t\t\t\tBradycardia, atrio-ventricular conduction block | \n\t\t\t\t\t\t\t\t\t8 g/kg i.v. | \n\t\t\t\t\t\t\t\t\tGill, 1982; Harvey, 1990 | \n\t\t\t\t\t\t\t\t
Tetrodotoxin (TTX) | \n\t\t\t\t\t\t\t\t\tBacteria: Pseudoalteromo-nas tetraodonis, certain species of Pseudomonas and Vibrio | \n\t\t\t\t\t\t\t\t\theterocyclic, organic, water-soluble non-protein molecule | \n\t\t\t\t\t\t\t\t\tVoltage dependent Na+ channels | \n\t\t\t\t\t\t\t\t\tShorten the AP duration and decrease the initial depolarizing phase of the AP | \n\t\t\t\t\t\t\t\t\tCardiac arrest | \n\t\t\t\t\t\t\t\t\t10.7 g/kg i.p.; 12.5 g/kg s.c.; 532 g/kg i.g. | \n\t\t\t\t\t\t\t\t\tMebs & Hucho, 1990; Xu et al., 2003 | \n\t\t\t\t\t\t\t\t
Saxitoxin | \n\t\t\t\t\t\t\t\t\tMarine dinoflagellates (Alexandrium sp., Gymnodinium sp.) and cyanobacteria (Anabaena sp., some Aphanizomenon spp., Cylindrospermopsis sp.) | \n\t\t\t\t\t\t\t\t\tHeterocy-clic guanidine | \n\t\t\t\t\t\t\t\t\tVoltage-gated Na+ channels- block L-type Ca2+ channels- partial block | \n\t\t\t\t\t\t\t\t\tShorten the AP duration and decrease the initial depolarizing phase of the AP | \n\t\t\t\t\t\t\t\t\tProlongation of P-Q interval, first degree of atrio-ventricular block, ventricular fibrilation | \n\t\t\t\t\t\t\t\t\t3 – 10 µg/kg i.p. | \n\t\t\t\t\t\t\t\t\tAnderson, 2000; Su et al., 2003 | \n\t\t\t\t\t\t\t\t
Natural cardiotoxic toxins from microbes: source, structure, receptors, mode of action, effects on heart and toxicity; i.g.- intra-gastric administration
electrical activity is blocked leading to blockade of myocardium excitability and cardiac arrest, although sodium channels are usually not affected in case of intoxication.
\n\t\t\t\t\tAlgae are ubiquitous micro-organisms in aqueous environments. Some of them will periodically form harmful “blooms.” Karenia brevis is a dinoflagellate that can form harmful blooms known as “Florida red tides”. Blooms are associated with the production of a group of powerful neurotoxins known as brevetoxins.
\n\t\t\t\t\tBrevetoxin (PbTx) is produced by marine dinoflagellates. It is polyether neurotoxin that targets the voltage-gated sodium channels present in all excitable membranes including heart tissues. Brevetoxins open voltage-gated sodium ion channels in cell membranes and cause uncontrolled sodium influx into the cell leading to the depolarization (Purkerson et al., 1999). Humans can be exposed to PbTx by ingesting brevetoxin-contaminated shellfish or through other environmental exposures. Its affinity for the rat heart tissue is much lower in contrast to the heart tissue of marine animals, but comparable with the skeletal muscle and brain (Dechraoui et al., 2006). At least 10 different brevetoxins have been isolated from seawater blooms and K. brevis cultures. PbTx in a dose higher than 25 µg/kg produces heart block, ventricular extrasystoles and idioventricular rhythms in conscious rats. It was concluded that brevetoxin causes changes in the cardiac conduction system and multiple changes in the function of the nervous system (Templeton et al., 1989). Systemic accumulation of the toxin in artificially respirated cats injected with PbTx leads to cardiovascular collapse and death (Borison et al., 1985).
\n\t\t\t\t\tYessotoxins (YTXs) are polycyclic ether compounds produced by phytoplanktonic dinoflagellates (algal toxins). They can accumulate in shellfish which are a source of human intoxication through contaminated seafood ingestion. YTX, homoyessotoxin and 45-hydroxy-homoyessotoxin are lethal when administered intraperitonealy (i.p.) to mice. Although the mechanisms of the cardiotoxicity of YTX and homoyessotoxins are not well understood, some data from in vitro experiments, such as changes of intracellular calcium and cyclic AMP concentrations, alteration of cytoskeletal and adhesion molecules, caspases activation and opening of the permeability transition pore of mitochondria, support their cardiotoxic action (Dominguez et al., 2010; for a review see Tubaro et al., 2010). They induce microscopically visible ultrastructural changes in heart tissue after intraperitoneal and oral exposure. Noticeable intracytoplasmic oedema of cardiac muscle cells was observed within three hours after the i.p. administration of YTX at a dose of 300 g/kg or higher (Terao et al., 1990). In mice YTX produces swelling of cardiomyocytes and separation of organelles in the area near capillaries after oral (10 mg/kg) and i.p. (1 mg/kg) toxin administration (Aune et al., 2002).
\n\t\t\t\t\tCiguatera caused by fish poisoning is a foodborne disease caused by eating certain fishes whose meat is contaminated with ciguatoxins produced by dinoflagellates such as Gambierdiscus toxicus. These toxins include ciguatoxin (CTX), maitotoxin, scaritoxin and palytoxin. Ciguatera fish poisoning is primarily endemic in tropical regions of the world. On neuroblastoma cells, CTX induces a membrane depolarization which is due to an action that increases Na+ permeability and is prevented by voltage-gated sodium channel blocker TTX (Bidard et al., 1984). Intravenous injections of ciguatoxin evoke dose-dependent effects: bradycardia and atrioventricular conduction block at low doses, ventricular tachycardia at sublethal doses, and heart failure at high doses (up to 160 µg/kg) (Legrand et al., 1982). The Caribbean ciguatoxin (C-CTX-1) stimulates the release of acetylcholin (ACh) and produces muscarinic effect on frog atrial fibres (Sauviat, 1999; Sauviat et al., 2002).
\n\t\t\t\t\t\tName | \n\t\t\t\t\t\t\t\t\tSource (produced by) | \n\t\t\t\t\t\t\t\t\tChemical structure | \n\t\t\t\t\t\t\t\t\tTarget | \n\t\t\t\t\t\t\t\t\tMode of action | \n\t\t\t\t\t\t\t\t\tEffects | \n\t\t\t\t\t\t\t\t\tAcute LD50 in mice | \n\t\t\t\t\t\t\t\t\tReference | \n\t\t\t\t\t\t\t\t
Algal toxins | \n\t\t\t\t\t\t\t\t|||||||
Brevetoxin | \n\t\t\t\t\t\t\t\t\tDinoflagellate Karenia brevis \n\t\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\t\tCyclic polyether \n\t\t\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\t\t\tVoltage-gated Na+ channels | \n\t\t\t\t\t\t\t\t\tDepolari-zation, AP duration increase | \n\t\t\t\t\t\t\t\t\tHeart block, ventricular extrasystoles and idioventricular rhythms | \n\t\t\t\t\t\t\t\t\t250 µg/kg i.p. | \n\t\t\t\t\t\t\t\t\tPurkerson et al., 1999; Templeton et al., 1989; Selwood et al., 2008 | \n\t\t\t\t\t\t\t\t
Yes-sotoxins | \n\t\t\t\t\t\t\t\t\tAlgae | \n\t\t\t\t\t\t\t\t\tPolycyclic ether compo-unds | \n\t\t\t\t\t\t\t\t\tVoltage gated Ca2+ channels | \n\t\t\t\t\t\t\t\t\tReduction of the firing and biting frequency of rat cardiac cells | \n\t\t\t\t\t\t\t\t\tChanges of intracellular Ca2+ and cyclic AMP concentrations, alteration of cytoskeletal and adhesion molecules, caspases activation and opening of the permeability transition pore of mitochondria | \n\t\t\t\t\t\t\t\t\t444-512 µg/kg i.p. | \n\t\t\t\t\t\t\t\t\tTubaro et al., 2003; Dell’Ovo et al., 2008 | \n\t\t\t\t\t\t\t\t
Ciguatoxin | \n\t\t\t\t\t\t\t\t\tDinoflagellate Gambierdiscus toxicus | \n\t\t\t\t\t\t\t\t\tPolyether toxins | \n\t\t\t\t\t\t\t\t\tVoltage-gated Na+ channels | \n\t\t\t\t\t\t\t\t\tDepolari-zation, AP duration increase, arrhythmias | \n\t\t\t\t\t\t\t\t\tBiphasic inotropic and chronotropic excitatory, and inhibitory effects | \n\t\t\t\t\t\t\t\t\t0.3 – 10 µg/kg i.p. | \n\t\t\t\t\t\t\t\t\tDechraoui et al., 1999 | \n\t\t\t\t\t\t\t\t
Maitotoxin | \n\t\t\t\t\t\t\t\t\tDinoflagellate Gambierdiscus toxicus | \n\t\t\t\t\t\t\t\t\tN/A | \n\t\t\t\t\t\t\t\t\tCa2+ channels | \n\t\t\t\t\t\t\t\t\tAgonist | \n\t\t\t\t\t\t\t\t\tAP amplitude increase | \n\t\t\t\t\t\t\t\t\t0.17 mg/kg i.p. | \n\t\t\t\t\t\t\t\t\tIgarashi et al., 1999; Mebs & Hucho, 1990 | \n\t\t\t\t\t\t\t\t
Natural cardiotoxic toxins from algae: source, structure, receptors, mode of action, effects on heart and toxicity. (N/A - not applicable).
Maitotoxin (MTX) plays an important role in the syndrome named ciguatera poisoning. The toxin is derived from Gambierdiscus toxicus, a marine dinoflagellate species (for a review see Mebs & Hucho, 1990). MTX causes dose-dependent effects on the heart. It has positive inotropic effects on heart preparations and causes irreversible contracture of isolated rat cardiomyocytes that can be prevented by specific voltage-dependent Ca2+ channel blocker verapamil (Kobayashi et al., 1986). MTX increases dose-dependent increase in Ca2+ activity in freshly dispersed cardiomyocytes. This effect of MTX may be inhibited by reducing Ca2+ concentration in the culture medium or by the calcium-channel blocker verapamil. Therefore, it has been concluded that MTX specifically activates voltage-dependent Ca2+ channels. This influx of Ca2+ into the cells is considered an important mechanism for cardiotoxicity of the MTX (Santostasi et al., 1990).
\n\t\t\t\t\tAnimal venoms are usually a complex mixture of polypeptides, enzymes and molecules which can cause cell injury. Polypeptides exert their effect through action on ion channels and in a cell\'s plasma membrane. Enzymes can cause membrane lysis, pore formation, etc.
\n\t\t\tPalytoxin (PTX) was first toxin isolated from the soft coral Palythoa toxica. PTX is one of the most powerful marine biotoxins of a high molecular weight ( 3.3 kDa). It is the most potent non-proteinic and non-peptidic toxic substance known, with a lethal dose LD50 of 0.15 g/kg in mice by the i.v. route (Moore & Scheuer, 1971).
\n\t\t\tIberiotoxin (IbTX) is derived from the venom of Eastern Indian red scorpion Buthus tamulus. IbTX selectively inhibits current through the calcium-activated potassium channels. IbTX in a 2 M concentration increased the stimulation-induced ACh release (Kawada et al., 2010). It was reported that some patients who had been stung by a scorpion had signs such as hypertension and supraventricular tachycardia (Bawaskar & Bawaskar, 1992), to which may contribute also IbTX.
\n\t\t\tBatrachotoxins (BTXs) are neurotoxic steroidal alkaloids first isolated from a Colombian poison-dart frog. BTXs are lipid-soluble toxins that bind with a high affinity to the type 2 receptor site of voltage-gated sodium channels in nerve and muscle membranes, keeping them in an open state (Albuquerque et al., 1971; Huang et al., 1984). This results in cell depolarization since BTXs inhibit inactivation of sodium channels. BTXs seem to play the most important role in cardiotoxicity. The cardiotoxic effects of BTXs accompanied by arrhythmia and cardiac arrest are connected to the activation of voltage-gated sodium channels in cardiac cells (Mebs & Hucho, 1990). It can evoke premature heart beat and fatal ventricular fibrillation associated with the haemodynamic arrest (Albuquerque et al., 1971).
\n\t\t\tAtrotoxin (ATX) is isolated from a venomous rattlesnake species Crotalus atrox found in the United States and Mexico. ATX binds reversibly to the voltage-gated calcium channels, leading to the increase of voltage-dependent calcium currents in single, dispersed guinea pig ventricular cells. ATX acts as a specific Ca2+ channel agonist (Hamilton et al., 1985).
\n\t\t\tEquinatoxins are pore-forming proteins isolated from the sea anemone Actinia equine. First evidence that equinatoxins are cardiotoxic was provided by Sket et al. (1974) by administration of tentacle extract of sea anemone i.v. into rats. Later, the isolation of three cardiotoxic proteins named Equinatoxin I, II and III with median lethal doses of 23, 35 and 83 µg/kg in mice, respectively (Macek & Lebez, 1988), was reported. EqT II is a pore forming toxin that through de novo formed pores evokes significant increase of intracellular Ca2+ activity, which cannot be blocked by conventional sodium and calcium channel blockers and probably plays an important role in direct (cytotoxic) or indirect cardiotoxicity through coronary vessel contraction and drop of the coronary perfusion rate (Frangež et al., 2000; Frangež et al., 2008; Zorec et al., 1990). All three equinatoxins are highly haemolytic and can cause a dose-dependent increase in potassium activity in blood plasma, leading to arrhythmias and cardiac arrest. Administered i.v. they produce dose-dependent disturbances in electrical activity of the heart accompanied by blood pressure changes. Additional information about direct dose-dependent cardiotoxic effects of EQT IIs were provided from the experiments on Langendorff\'s heart preparations. It causes a concentration-dependent drop of the perfusion rate, decreases left ventricular pressure and produces arrhythmias followed by cardiac arrest (Bunc et al., 1999).
\n\t\t\tA cytolytic protein was isolated from the Indian monocellate cobra (Naja kaouthia) venom. Intraperitoneal median lethal dose was estimated to be 2.5 mg/kg in Balb/C in male mice. In vitro the toxin produces auricular blockade as shown on isolated guinea pig auricle (Debnath et al., 2010).
\n\t\t\tTaicatoxin (TCX) is a snake toxin derived from the Australian taipan snake Oxyuranus scutellatus scutellatus. TCX reversibly and specifically blocks voltage-dependent L-type calcium channels in nanomolar concentrations (Brown et al., 1987). TCX decreases the plateau of AP in cardiomyocytes leading to a decrease in contractility. TCX has a negative chronotropic effect and evokes arrhythmias (Fantini et al., 1996). Electrocardiographic abnormalities were described in patients envenomed with a number of different species including Oxyuranus spp. Electrocardiographic changes include septal T wave inversion and bradycardia, and atrioventricular block. One of possible mechanisms which might be responsible for such clinical signs is a calcium channel blockade on cardiomyocytes (Lalloo et al., 1997).
\n\t\t\tConotoxins are peptides derived from the marine snail Conus geographus and consist of 10 to 30 amino acid residues. Many of these peptides modulate the activity of different ion channels. ω-conotoxin inhibits N-type voltage-dependent Ca2+ channels. It decreases the magnitude of cardiac AP and possesses a negative inotropic effect (Nielsen, 2000).
\n\t\t\tCrotoxin (CTX) is derived from the venom of the South American rattlesnake, Crotalus durissus terrificus. In vitro, CTX decreases contractile force, increases the P-R interval and displaces the S-T segment. Arrhythmias are uncommon. The reduction of the contractile force and the increase in creatine kinase (CK) activity are ascribed to the release of free fatty acids and lysophospholipids, and to a cellular lesion (Santos et al., 1990; Zhang et al., 2010).
\n\t\t\tSarafotoxins (SRTs) and bibrotoxins are a group of extremely poisonous cardiotoxic snake venom peptides that show a striking structural similarity to endothelins (Becker et al., 1993; Kloog et al., 1988). SRTs are highly lethal peptides: in mice, the LD50 is 15 µg/kg body weight equalling the LD50 for endothelin (Bdolah et al., 1989), which is quite surprising for a peptide naturally occurring in the plasma of healthy humans. Sarafotoxin S6C, the most acidic endothelin-like peptide, shows reduced vasoconstrictive potency and is a highly selective natural ETBR agonist (over 100 000 times higher affinity for the ETBR vs. the ETAR; [Williams et al., 1991]).
\n\t\t\tGs-Mtx-4 is an amfipathic peptide toxin derived from the venom of the tarantula spider (Grammostola spatulata) with a molecular weight of 4 kDa (Hodgson & Isbister, 2009). It is the only toxin known that specifically affects cationic stretch activated ion channels and is therefore able to inhibit atrial fibrillation (Bowman et al., 2007).
\n\t\t\tSome of the natural toxins acting on the cardiovascular system are very potent and highly specific for some receptors in cardiac and neuronal tissue. They can block, activate and even modulate the ion channels activity in excitable membranes. Although they are very stable molecules and possess high receptors specificity, they are seldom used as therapeutic drugs. Information about their three dimensional structure and data from structure-function studies of protein toxins may provide useful information for synthesis of smaller analogues with lower toxicity. Few natural toxins have potential in clinical use for treatment of cardiovascular dysfunction. Some of them have a positive inotropic effect, i.e. grayanotoxin, veratridine (Brill & Wasserstrom, 1986; Tirapelli et al., 2008). Due to their high toxicity, none of the described natural cardiotoxic substances are used as therapeutic drugs for treating cardiovascular diseases. Recently, sarafotoxins have been utilized to develop new, low molecular weight substances with metalloproteinase inhibitory activity. The modified molecule of the sarafotoxin 6b is used as a starting point, which has retained metalloproteinase inhibitory activity and removed vasoconstrictor activity. From this, the peptide (STX-S4-CT) was developed, which will hopefully provide a foundation for further development of improved candidate molecules (Hodgson & Isbister, 2009). Some promising
\n\t\t\tName | \n\t\t\t\t\t\tSource (produced by) | \n\t\t\t\t\t\tChemical structure | \n\t\t\t\t\t\tTarget | \n\t\t\t\t\t\tMode of action | \n\t\t\t\t\t\tEffects | \n\t\t\t\t\t\tAcute LD50 in mice | \n\t\t\t\t\t\tSource | \n\t\t\t\t\t
Animal toxins | \n\t\t\t\t\t|||||||
Palytoxin | \n\t\t\t\t\t\tSoft coral: Palythoa toxica | \n\t\t\t\t\t\tAliphatics carbon chain containing a series of heterocyclic rings | \n\t\t\t\t\t\tNa+/K+-ATPase; Hemolysin | \n\t\t\t\t\t\tVoltage-dependent K+ channels | \n\t\t\t\t\t\tHaemolysis, arrhythmias | \n\t\t\t\t\t\t0.15 µg/kg | \n\t\t\t\t\t\tSosa et al., 2009 | \n\t\t\t\t\t
Equinatoxin I, II, II | \n\t\t\t\t\t\tSea anemone: Actinia equina | \n\t\t\t\t\t\tProteins | \n\t\t\t\t\t\tHaemolysin | \n\t\t\t\t\t\tNew cation non-selective pore formation | \n\t\t\t\t\t\tDose-dependent arrhythmias, cardiac arrest, haemolysis | \n\t\t\t\t\t\t25,30 and 83 µg/kg i.v. | \n\t\t\t\t\t\tMaček & Lebez, 1988; Sket et al., 1974 | \n\t\t\t\t\t
Batrachotoxins (BTX) | \n\t\t\t\t\t\tSome frogs species (poison-dart frog), melyrid beetles and birds (Ifrita kowaldi, Colluricincla megarhyncha) | \n\t\t\t\t\t\tSteroidal alkaloids | \n\t\t\t\t\t\tNa+ channels | \n\t\t\t\t\t\tDepolarize, lengthen the AP | \n\t\t\t\t\t\tArrhythmias, extrasystoles, ventricular fibrillation | \n\t\t\t\t\t\t2 µg/kg s.c. | \n\t\t\t\t\t\tAlbuquerque et al., 1971; Mebs & Hucho, 1990 | \n\t\t\t\t\t
Atrotoxin | \n\t\t\t\t\t\tSnake: Crotalus atrox | \n\t\t\t\t\t\tN/A | \n\t\t\t\t\t\tCa2+ channels | \n\t\t\t\t\t\tAgonist, AP amplitude increase | \n\t\t\t\t\t\tArrhythmias | \n\t\t\t\t\t\t89.4 – 137 µg i.v. | \n\t\t\t\t\t\tHamilton et al., 1985; Barros et al., 1998 | \n\t\t\t\t\t
Cardiotoxic-cytotoxic protein (MW 6.76 kDa) | \n\t\t\t\t\t\tIndian monocellate cobra (Naja kaouthia) | \n\t\t\t\t\t\tProtein | \n\t\t\t\t\t\tHeart | \n\t\t\t\t\t\tSinuauricular blockade | \n\t\t\t\t\t\tArrhythmias | \n\t\t\t\t\t\t2.5 mg/kg i.p. | \n\t\t\t\t\t\tDebnath et al., 2010 | \n\t\t\t\t\t
Taicatoxin (TCX) | \n\t\t\t\t\t\tAustralian taipan snake Oxyuranus scutellatus | \n\t\t\t\t\t\tN/A | \n\t\t\t\t\t\tCa2+ channels | \n\t\t\t\t\t\tAntagonist | \n\t\t\t\t\t\tBradycardia, atrioventricular block | \n\t\t\t\t\t\tN/A | \n\t\t\t\t\t\tBrown et al., 1987; Lalloo et al., 1997 | \n\t\t\t\t\t
Omega-conotoxin | \n\t\t\t\t\t\tCone snail from genus Conus | \n\t\t\t\t\t\tPeptide | \n\t\t\t\t\t\tN-type voltage-dependent Ca2+ channels | \n\t\t\t\t\t\tAntagonist | \n\t\t\t\t\t\tDecreases the magnitude of AP plateau, negative inotropic effects | \n\t\t\t\t\t\tN/A | \n\t\t\t\t\t\tNielsen, 2000 | \n\t\t\t\t\t
Crotoxin (CTX) | \n\t\t\t\t\t\tSouth American rattlesnake (Crotalus durissus terrificus) | \n\t\t\t\t\t\tProtein; crotapotin basic phospolipase A2 | \n\t\t\t\t\t\tL-type Ca2+ channels | \n\t\t\t\t\t\tAgonist | \n\t\t\t\t\t\tElongation of AP duration, an increase of its amplitude | \n\t\t\t\t\t\t55.5 – 70.5 µg/kg i.p. | \n\t\t\t\t\t\tRangel-Santos et al., 2004 | \n\t\t\t\t\t
Sarafotoxin (SRTs) and bibrotoxin | \n\t\t\t\t\t\tSnake: Atractaspis engaddensis | \n\t\t\t\t\t\tPeptide | \n\t\t\t\t\t\tEndothelin receptors | \n\t\t\t\t\t\tAgonist | \n\t\t\t\t\t\tArrhythmias | \n\t\t\t\t\t\t15 µg/kg | \n\t\t\t\t\t\tBdolah et al., 1989 | \n\t\t\t\t\t
GsMtx-4 | \n\t\t\t\t\t\tSpider – tarantula: Grammostola spatulata | \n\t\t\t\t\t\tPeptide | \n\t\t\t\t\t\tStretch activated ion channels (SACs) | \n\t\t\t\t\t\tAntagonist | \n\t\t\t\t\t\tInhibits atrial fibrillation | \n\t\t\t\t\t\tN/A | \n\t\t\t\t\t\tBowman et al., 2007 | \n\t\t\t\t\t
Natural cardiotoxic toxins from animals: source, structure, receptors, mode of action, effects on heart and toxicity. (N/A - not applicable).
results in the treatment of cardiovascular disorders were also obtained with GsMtx-4 toxin isolated from tarantula Grammostola spatulata venom. This toxin is able to inhibit the stretch activated ion channels (SACs) and consequently inhibits atrial fibrillation. Due to its described properties, it can be used as a framework for developing a new class of anti-arrhythmic drugs, which would be directed against pathophysiologic mechanisms of atrial fibrillation, instead of just dealing with the symptoms as with many current therapies (Hodgson & Isbister, 2009).
\n\t\tSevere acute toxic insult caused by natural toxins can cause functional changes in heart tissue physiology or even cardiac cell death. Most of the natural toxins derived from plants, bacteria, phytoplanktonic dinoflagellates, fungi and animals target ionic channels in excitable membranes of cardiac cells or cardiac cell membranes itself, produce alteration in AP (e.g. depolarization, repolarization, alterations in its duration) or significant changes in intracellular ion activity. These changes may lead to reversible or even irreversible life threatening cardiac arrhythmias and eventually heart failure.
\n\t\tDuring an event of earthquake stability of dams is of paramount importance as their failure can cause immense property and environmental damages. When dam-reservoir-foundation system is subjected to the dynamic loading it causes a coupled phenomenon; ground motion and deformations in the dam generate hydrodynamic pressure in the reservoir, which, in turn, can intensify the dynamic response of the dam. Moreover, spatial-temporal variation of stresses in the dam-body depends on the dynamic interactions between the dam, reservoir, and foundation. Therefore, it becomes necessary to use numerical techniques for the safety assessment of a given dam-design against a particular ground motion.
\nDynamic finite element method is the most extended approach for computing the seismic response of the dam-reservoir system to the earthquake loading [1]. In this approach finite elements are used for discretization of space domain, and basis functions are locally supported on the spatial domain of these elements and remain independent of time. Furthermore, nodal values of primary unknowns depend only on time. Accordingly, this arrangement yields a system of ordinary differential equations (ODEs) in time which is then solved by employing time-marching schemes based on the finite difference method (FDM), such as Newmark-
In dynamic finite element method (FEM), it is desirable to adopt large time-steps to decrease the computation time while solving a transient problem. Therefore, it is imperative that the time-marching scheme remains unconditionally stable and higher order accurate [1]. In addition, it should filter out the high frequency components from the response of structure. To achieve these goals, Hughes and Hulbert presented space-time finite element method (ST/FEM) for solving the elastodynamics problem [2]. In this method, displacements
However, for elastodynamics problem, ST/FEM, yields a larger system of linear equations due to due to the time-discontinuous interpolation of displacement and velocity fields. Several efforts have been made in the past to overcome this issue; both explicit [8] and implicit [9] predictor-multi-corrector iteration schemes have been proposed to solve linear and nonlinear dynamics problems. Recently, to reduce the number of unknowns in ST/FEM, a different approach is taken in which only velocity is included in primary unknowns while displacement and stresses are computed from the velocity in a post-processing step [4, 10]. To this end, the objective of the present chapter is to introduce this method (henceforth, ST/FEM) in a pedagogical manner. The rest of the chapter is organized as follows. Sections 2 and 3 deal with the fundamentals of time-discontinuous Galerkin method. Section 4 describes the dam-reservoir-soil interaction problem, and Section 5 discusses the application of ST/FEM for this problem. Lastly, Section 6 demonstrates the numerical performance of proposed method and in the last section concluding remarks are included.
\nConsider a mass-spring-dashpot system as depicted in Figure 1. The governing equation of motion is described by the following second order initial value problem in time.
\nSchematic diagram of the mass-spring-dashpot system.
where
In what follows, this second order ODE will be utilized to discuss the fundamental concepts behind time-discontinuous Galerkin methods (henceforth, tDGM).
\nIn two-field tDGM (henceforth, uv-tDGM), both displacement (
Schematic diagram of time discontinuous approximation: (a) piecewise linear interpolation, and (b) piecewise quadratic interpolation.
where
\nare the discontinuous values of
The weak-form of the uv-tDGM can be stated as: find
where
Eq. (10) denotes that, in uv-tDGM, displacement-velocity compatibility relationship is satisfied in weak form.
\nTo decrease the number of unknowns in comparison to those involved in uv-tDGM, displacement-velocity compatibility condition (cf. Eq. 6) can be explicitly satisfied and velocity can be selected as primary unknown. Henceforth, this strategy will be termed as v-tDGM. In v-tDGM,
The weak form of the v-tDGM reads: Find
Note that Eqs. (9) and (11) are identical, however, in former,
Let us now focus on the discretization of weak-form (cf. Eq. (11)) by using the locally defined piecewise linear test and trial functions,
\nwhere
\nAccordingly, Eq. 11 transforms into following matrix-vector form.
\nwhere
In this section, numerical analysis of the tDGM schemes, (viz. uv-tDGM and v-tDGM) for the second order ODE will be performed. To assess the stability characteristics and temporal accuracy of these schemes, classical finite difference techniques will be used ([11], Chapter 9). In this context, it is sufficient to consider the following homogeneous and undamped form of Eq. (1):
\nIn this section it will be shown that v-tDGM is a true energy-decaying scheme. Consider Eq. (17) which represents the governing equation of a spring-mass system. The total energy (sum of kinetic and potential energy) of the system remains constant because damping and external forces are absent in the system.
\nConsider the time domain
Accordingly, it can be shown that
\nor
\nThis shows that v-tDGM is an energy decaying time integration algorithm, in which the total energy during any time step,
To assess the energy dissipation characteristics of v-tDGM, Eq. (17) is solved with
Energy decay characteristics of v-tDGM; (a) temporal variation of normalized total energy and (b) phase diagram obtained with different time-step sizes.
In this section, to study the stability characteristics of v-tDGM, Eq. (17) is considered. The matrix-vector form corresponding to this problem is given by
\nwhere
where
To investigate the stability of v-tDGM one should look into the eigenvalues of
Figure 4 plots the frequency responses of
Frequency response of spectral radius ρ for v-tDGM.
In [4], it is shown that
where
Subsequently, by expanding
A direct consequence of the convergence is that the solution of Eq. (17) can be given by following expression [1]:
\nwith
\nwhere
Further, to investigate the accuracy of v-tDGM, algorithmic damping ratio, which is a measure of amplitude decay, and relative frequency error
Accuracy of v-tDGM: (a) algorithmic damping ratio, and (b) relative frequency error in low frequency regime (after [4]).
A dam-reservoir-soil (DRS) system which is subjected to the spatially uniform horizontal (
Schematic diagram of dam-reservoir-soil (DRS) system subjected to seismic ground motion.
Further, hydrodynamic pressure distribution in the reservoir is modeled by the pressure wave equation,
\nwith following initial and boundary conditions.
\nIn Eq. (26),
Let us now consider the initial-boundary value problem of the solid domain which is described by,
\nFurthermore, following time dependent boundary conditions will be considered in Eq. (33):
\nIn addition, solid domain is considered to be an isotropic, homogeneous, linear elastic material with
\nIn Eqs. (31)–(34),
in which,
Recently, ST/FEM is employed to solve dam-reservoir-soil interaction problem [10] in which the resultant matrix-vector form is given by
\nwhere
Further, In Eqs. (41) and (42),
\nwhere
\ndenote mass matrix, diffusion matrix, and viscous boundary at the upstream truncated boundary, respectively. The fluid-solid coupling matrix
and right hand side spatial nodal vectors in Eqs. (41) and (42) becomes,
\nwhere
in which
the solid-fluid coupling matrix,
\nand right hand side spatial nodal vectors is given by,
\nwhere
Further, the force vector
Lastly, nodal values of displacement and pressure field at time
In this section, ST/FEM with block iterative algorithm has been employed to study the response of the concrete gravity dam to the horizontal earthquake motion (see [10]). In the numerical modeling two cases are considered; (i) dam-reservoir (DR) system, in which foundation is considered to be rigid, and (ii) dam-reservoir-soil (DRS) system, in which the foundation is an elastic deformable body.
\nFigure 7 depicts the physical dimensions of the dam-reservoir system. Length of the reservoir in upstream direction is
Physical dimensions of dam-reservoir system (after [10]).
Figure 8 represents the accelerogram (horizontal component) recorded at a control point on the free surface; the maximum and minimum values of acceleration are
Time history of horizontal component of ground motion recorded at free-surface.
Acceleration response at the crest of dam in DR and DRS system; time history of (a) horizontal component and (b) vertical component of acceleration, and Fourier spectrum of (c) horizontal component and (d) vertical component of acceleration (after [10]).
Interestingly, in both cases, it is observed that the critical location for pressure is at the base of the dam. Figure 10 presents the evolution of
Temporal response of (a) normalized hydrodynamic pressure, (b) principal tensile stress and (c) principal compressive stress at the base of dam in DR and DRS system (after [10]).
(a) and (c): Hydrodynamic pressure field in the reservoir, and (b) and (d): magnified deformed configuration of dam at times t = 18:02 s and t = 18:08 s (after [10]).
In this chapter, novel concepts of time-discontinuous Galerkin (tDGM) method is presented. A method called v-tDGM is derived to solve second order ODEs in time. In this method velocity is the primary unknown and it remain discontinuous at discrete times. Thereby, the time-continuity of velocity is satisfied in a weak sense. However, displacement is obtained by time-integration of the velocity in a post-processing step by virtue of which it is continuous in time. It is demonstrated that the present method is unconditionally stable and third-order accurate in time for linear interpolation of velocity in time. Therefore, it can be stated that the numerical characteristics of the v-ST/FEM scheme, therefore, make it highly suitable for computing the response of bodies subjected to dynamic loading conditions, such as fast-moving loads, impulsive loading, and long-duration seismic loading, among others.
\nSubsequently, ST/FEM is used to compute the response of a dam-reservoir-soil (DRS) system to the earthquake loading while considering all types of dynamic interactions. An auxiliary variable
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