Dr. Pletser’s experience includes 30 years of working with the European Space Agency as a Senior Physicist/Engineer and coordinating their parabolic flight campaigns, and he is the Guinness World Record holder for the most number of aircraft flown (12) in parabolas, personally logging more than 7,300 parabolas.
\\n\\n
Seeing the 5,000th book published makes us at the same time proud, happy, humble, and grateful. This is a great opportunity to stop and celebrate what we have done so far, but is also an opportunity to engage even more, grow, and succeed. It wouldn't be possible to get here without the synergy of team members’ hard work and authors and editors who devote time and their expertise into Open Access book publishing with us.
\\n\\n
Over these years, we have gone from pioneering the scientific Open Access book publishing field to being the world’s largest Open Access book publisher. Nonetheless, our vision has remained the same: to meet the challenges of making relevant knowledge available to the worldwide community under the Open Access model.
\\n\\n
We are excited about the present, and we look forward to sharing many more successes in the future.
\\n\\n
Thank you all for being part of the journey. 5,000 times thank you!
\\n\\n
Now with 5,000 titles available Open Access, which one will you read next?
Preparation of Space Experiments edited by international leading expert Dr. Vladimir Pletser, Director of Space Training Operations at Blue Abyss is the 5,000th Open Access book published by IntechOpen and our milestone publication!
\n\n
"This book presents some of the current trends in space microgravity research. The eleven chapters introduce various facets of space research in physical sciences, human physiology and technology developed using the microgravity environment not only to improve our fundamental understanding in these domains but also to adapt this new knowledge for application on earth." says the editor. Listen what else Dr. Pletser has to say...
\n\n\n\n
Dr. Pletser’s experience includes 30 years of working with the European Space Agency as a Senior Physicist/Engineer and coordinating their parabolic flight campaigns, and he is the Guinness World Record holder for the most number of aircraft flown (12) in parabolas, personally logging more than 7,300 parabolas.
\n\n
Seeing the 5,000th book published makes us at the same time proud, happy, humble, and grateful. This is a great opportunity to stop and celebrate what we have done so far, but is also an opportunity to engage even more, grow, and succeed. It wouldn't be possible to get here without the synergy of team members’ hard work and authors and editors who devote time and their expertise into Open Access book publishing with us.
\n\n
Over these years, we have gone from pioneering the scientific Open Access book publishing field to being the world’s largest Open Access book publisher. Nonetheless, our vision has remained the same: to meet the challenges of making relevant knowledge available to the worldwide community under the Open Access model.
\n\n
We are excited about the present, and we look forward to sharing many more successes in the future.
\n\n
Thank you all for being part of the journey. 5,000 times thank you!
\n\n
Now with 5,000 titles available Open Access, which one will you read next?
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1. Introduction
The largest research object of modern perinatology and neonatology is preterm and growth retarded children. Despite the rapid development of perinatal care and the early prevention of many pathologies, worldwide perinatal morbidity and mortality remain high [1, 2, 3, 4].
The results of the scientific researches prove that perinatal pathologies play a leading role in the formation of illness, death, disability, social and biological disarray, and different types of neurodevelopmental disorders [5, 6, 7, 8, 9, 10]. It is known that birth is a complicated biological process regulated by numerous signal molecules and biologically active substances. The fetal inflammatory response plays a major role in the pathogenesis of premature birth [11]. In addition to prematurity, the hypoxic-ischemic changes in feto-placental system can result in different perinatal pathologies, such as acute intraventricular bleeding, periventricular leukomalation, necrotic enterocolitis, bronchial lung dysplasia, myocardial dysfunction, sepsis, etc. [12, 13, 14, 15].
Uteroplacental ischemia and circulatory changes in maternal-fetal system are the main chain in formation intrauterine hypoxia and different perinatal pathologies [16, 17, 18]. Previous investigations confirmed the significant role of endothelial function in the formation of different pregnancy pathologies and birth defects [19, 20, 21, 22]. The pathogenetic mechanisms of the formation of endothelial dysfunction during uteroplacental ischemia have not yet been investigated. Present chapter explores the role of vascular tone regulators of endothelial genesis in formation of microcirculatory and ischemic changes in preterm infants.
2. The pathophysiology of brain injury in hypoxic: ischemic encephalopathy (HIE)
Adaptation of the child to the extrauterine life significantly depends on the morpho-functional maturity of the organism, and it is more intense and more complicated in preterm babies than mature children [23, 24, 25].
The progress of all complicated pathophysiologic processes occurring in the newborn after birth significantly depends on cardiorespiratory adaptation [23, 24]. The changes in the cardiovascular and respiratory functions in the body related to the primarily changes in the microcirculation [25]. Microcirculatory changes are not only clinical symptoms of various pathologies of perinatal period but also one of the major factors that aggravate their course [26, 27].
HIE is one of the most serious birth complications accompanying with microcirculatory changes of different severity [28]. The pathogenesis of vascular changes in preterm infants is quite complicated and involves series of biochemical and molecular reactions (Figure 1). Persistent membrane depolarization results in excessive presynaptic glutamate release which follows with a series of cellular changes. The activation of NMDA receptors stimulates profound Ca2+ influx, which mediates cascades to cell death. Primary energy failure associated with the depletion of oxygen prevents oxidative phosphorylation, and the disrupting Na-K pump activity is followed by anaerobic metabolism with accumulation of lactic acid. With the restoration of blood flow, there is a brief period of normalization of cerebral metabolism called a latent period. The reperfusion is necessary for the recovery and stopping of processes leading to necrotic neuronal injury during the primary phase of injury. However when the brain has not recovered from the initial injury, the reperfusion can simultaneously cause additional (delayed) injury, and mitochondrial dysfunction continues. When cerebral ischemia is more acute and prolonged, especially in the result of accompanying pathological processes (infection, hereditary factors, environmental and other damaging factors), primary injury is followed by secondary injury, which is often characterized by subsequent resulting in more serious neurological and somatic disintegration in development [29]. Secondary injury is often associated with edema of the brain cells. Compensatory restoration of energy reactions is followed by the intracellular edema and by more complex inflammatory response cascade with the presence of free oxygen radicals [30].
Figure 1.
The pathogenesis of hypoxic-ischemic encephalopathy [33].
Increased amount of free radicals and nitric oxide (NO), increased synthesis of nitric oxide synthase (NOS), activated intercellular adhesion, and apoptosis are the tightly connected chains of this pathological process (10–13). However it is confirmed that endothelial NOS (eNOS) genesis plays very important role in maintaining pulmonary blood flow and preventing pulmonary hypertension. Some experimental studies suggested that inhibiting NOS could prevent further brain injury [31]. Selective inhibition of NO of neuronal genesis is more promising in the direction of pathogenetic treatment of HIE in newborn infants [31, 32, 33].
The severity of inflammatory processes is correlated with the activation of different mediators, especially cytokines and adhesion molecules. These molecules cause to the migration of leukocytes to the inflammation center and compact adhesion of migrated leukocytes to vascular endothelium [34, 35]. The main stimulus factor for the synthesis of inflammatory mediators is the activation of endothelial cells of the fetus. Thus, endothelial dysfunction is the main factor that stimulates intracellular and vascular adhesion and leads to the activation of fetal leukocytes [36, 37].
There is much to be investigated how the inflammatory response to hypoxia is regulated and the complete role of different mediators as well as vasoregulatory, anti-inflammatory, and apoptosis molecules under physiological and pathological conditions is unknown. The goal of this chapter is to present the results of recent investigations about the role of vasoregulatory markers in the formation of microcirculatory disorders in hypoxic-ischemic encephalopathy of preterm infants.
3. Endothelial dysfunction and microcirculatory disorders in HIE of preterm infants
Several clinical and experimental studies confirmed the role of endothelial dysfunction in the pathogenesis of hypoxic-ischemic brain injury. The prospective clinical trial of Azerbaijan Medical University Neonatology group (ACTRN12612000342819) determined that the eNOS activity is declined in the background of increased NO concentrations depending on the severity of HIE [38].
The aim of the same study was also to study of the peripheral blood concentrations of vasoregulatory mediators of endothelial genesis in the pathogenesis of microcirculatory changes in newborn children with the birth asphyxia. It investigated 240 preterm infants with a high risk of HIE during early neonatal period. The main groups of children were classified into four groups depending on the degree of the microcirculation changes. The first group included preterm infants without microcirculatory changes of the body. The children with mild-degree microcirculatory disorders (continued less than 1 day and self-regenerating peroral and acrocyanosis, capillary refilling time duration less than 3 s) were included in the second group. The third group consisted of children with moderate microcirculatory disorders (such as peroral and acrocyanosis, marbling of the skin, capillary refilling time up to 7 s and continuing from 1 day up to 3 days). The fourth group consisted of children with severe microcirculatory disorders (acute peroral and acrocyanosis, marbling of the skin continuing more than 3 days, capillary refilling time with the duration of more than 7 s and continuing more than 3 days). The parameters were compared with the data of 2 control groups, which consisted of infants without perinatal and neonatal pathologies: 22 healthy preterm infants were included in control 1 and 30 healthy term infants in control 2.
Depending on the magnitude of the microcirculatory defects, the levels of vasoregulatory markers included in the study is shown in Table 1. The statistically significant reduction in eNOS activity in the first few days of life is noticeable, depending on the degree of severity of the microcirculatory disturbances. However toward the end of the early neonatal period in mild and moderate group children, eNOS concentrations significantly increased compared with children with severe microcirculatory changes and control groups.
Table 1.
The level of vasoregulatory indicators in microcirculatory disturbances in children with HIE risk (p<0,05 in comparison with children with 0-none of, 1- mild, 2-moderate, 3-severe microcirculatory changes, and with # - Control 1, ^ - Control 2 infants).
As shown in Table 1, during severe microcirculation defects, NO synthesis of vascular endothelium remains at very low levels. In contrast, NO levels in the early days of the neonatal period were noted to significantly increase in infants with severe microcirculatory disturbances, and in the dynamics of the neonatal period, regardless of the microcirculatory changes severity, it is observed the increase of NO concentrations. At the same time, vasoconstrictor endothelin-1 levels rise during mild and moderate grades of microcirculation changes, while in infants with severe changes, it is reduced. This also proves once again that severe microcirculation disturbances lead to a violation of blood supply both in peripheral and vital organs during acute brain damage. We suggest that the lack of adequate levels of endothelin-1 synthesis, which is vasoconstrictor mediator of vascular endothelium in addition to decreased endothelial NOS activity, becomes one of the main points in the pathophysiology of HIE in preterm infants.
The follow-up results of these children included in this study identified significant relationships between peripheral endothelial vasoregulatory markers in the perinatal period and the formation of developmental disorders at an early age [39]. It was found that, in the presence of high concentrations of NO, early eNOS activity was insufficient in infants with moderate-to-severe neurodevelopmental disorders compared to neonates with mild neurologic changes or without evidence of neurological impairment (Table 2). These findings suggest that depressed eNOS activity and increased non-endothelial NO synthesis play also important roles in the formation of developmental impairments.
Table 2.
Blood concentrations of vasoregulatory markers in the early neonatal period by study groups. 1st group: HIE infants diagnosed with moderate-to-severe neurodevelopmental disorders or cerebral palsy; 2nd group: HIE infants with mild neurologic changes at an early age; 3rd group: HIE infants without evidence of neurological impairment in the post-neonatal period; control group: healthy preterm infants. ap<0,05 is considered statistically significant between main groups (1-2, 1-3, 2-3), and between main and control groups (1-c, 2-c, 3-c).
It is known that there is a disturbance of vasoregulation in the pathogenesis of various pathologies of the HIE and prenatal period [40, 41, 42]. Depending on the complexity of the pathological process and the degree of morphologic and functional immaturity of the body, hypoxic-ischemic lesions can lead to generalized system damage from mild to generalized severe dysfunctions and changes [43, 44, 45, 46, 47]. Acceleration of blood supply to vital organs during HIE is accompanied by peripheral vasospasm. However, the depletion of vascular tone’s regulating mechanisms during the severe and long-lasting processes leads to the tissue hypoxia and acidosis [40, 41, 42, 43, 44, 45, 46, 47]. This often leads to changes in vital organs, especially in brain tissue whose results are with changes that cannot be restored.
It is considered that statistically significant increase of NO levels in peripheral blood circulation during severe hypoxic changes is due to the exhaustion of endothelial NOS sources and the activation of non-endothelial NO synthesis sources. It is likely that in high endothelin-1 levels in children, mild and moderate changes are likely to compensate for an increase in peripheral vein tone and vital organs to maintain normal blood circulation. Reduced vasoconstrictor endothelium-1 levels in children with severe HIE symptoms are likely to be associated with decreased vascular tone and tissue hypoperfusion. In conclusion, the changes of capillary blood circulation in the result of endothelial dysfunction have the main role in the pathogenesis of hypoxic-ischemic inflammation in preterm infants.
Acknowledgments
The authors sincerely thank Science Development Foundation under the President of the Azerbaijan Republic for providing specific reagent kits (Grant SDF-2010-1(1)-40/28-M-2). We also thank the staff of the Clinical Biochemistry Laboratory of Azerbaijan Medical University for assistance with biomarker analysis.
Conflict of interest
The authors declare no conflict of interests.
\n',keywords:"microcirculation, hypoxic encephalopathy, preterm infants, endothelial function, nitric oxide",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/69823.pdf",chapterXML:"https://mts.intechopen.com/source/xml/69823.xml",downloadPdfUrl:"/chapter/pdf-download/69823",previewPdfUrl:"/chapter/pdf-preview/69823",totalDownloads:177,totalViews:0,totalCrossrefCites:0,dateSubmitted:"March 30th 2019",dateReviewed:"September 25th 2019",datePrePublished:"October 30th 2019",datePublished:null,dateFinished:null,readingETA:"0",abstract:"Endothelial function plays an important role in the extrauterine adaptation of newborn infants. Endothelium produces different biologically active mediators, which play the central role in physiological and pathological processes and also in the extrauterine adaptation of newborn infants. The imbalance between vasoconstrictive and vasodilatation factors results in impaired cardiovascular adaptation and microcirculation and also brain injury. Microcirculatory disturbances are observed very often in preterm babies, who have a serious risk for perinatal brain injury and further neurodevelopment disabilities. Present chapter presents the pathogenetic role of vascular tone regulators of endothelial genesis in the formation of microcirculatory changes in preterm babies with a high risk of perinatal hypoxic encephalopathy.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/69823",risUrl:"/chapter/ris/69823",signatures:"Saadat Huseynova, Jamila Gurbanova, Afat Hasanova, Samaya Alizada and Nushaba Panakhova",book:{id:"7842",title:"Basic and Clinical Understanding of Microcirculation",subtitle:null,fullTitle:"Basic and Clinical Understanding of Microcirculation",slug:"basic-and-clinical-understanding-of-microcirculation",publishedDate:"July 22nd 2020",bookSignature:"Kaneez Fatima Shad, Seyed Soheil Saeedi Saravi and Nazar Luqman Bilgrami",coverURL:"https://cdn.intechopen.com/books/images_new/7842.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"31988",title:"Prof.",name:"Kaneez",middleName:null,surname:"Fatima Shad",slug:"kaneez-fatima-shad",fullName:"Kaneez Fatima Shad"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:null,sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. The pathophysiology of brain injury in hypoxic: ischemic encephalopathy (HIE)",level:"1"},{id:"sec_3",title:"3. Endothelial dysfunction and microcirculatory disorders in HIE of preterm infants",level:"1"},{id:"sec_4",title:"Acknowledgments",level:"1"},{id:"sec_7",title:"Conflict of interest",level:"1"}],chapterReferences:[{id:"B1",body:'Lees C, Marlow N, Arabin B, Bilardo CM, Brezinka C, Derks JB, et al. Perinatal morbidity and mortality in early-onset fetal growth restriction: Cohort outcomes of the trial of randomized umbilical and fetal flow in Europe (TRUFFLE). Ultrasound in Obstetrics & Gynecology. 2013;42:400-408'},{id:"B2",body:'Unterscheider J, Daly S, Geary MP, Kennelly MM, McAuliffe FM, O’Donoghue K, et al. Optimizing the definition of intrauterine growth restriction: The multicenter prospective PORTO study. 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Uteroplacental ischemia in early- and late-onset pre-eclampsia: A role for the fetus? Ultrasound in Obstetrics & Gynecology. 2012;40(4):373-382'},{id:"B18",body:'Warrington J, Fan F, Murphy S, Roman R, Drummond H, Granger J, et al. Placental ischemia impairs cerebral blood flow autoregulation and increases blood-brain barrier permeability in pregnant rats. The FASEB Journal. 2015;29(1 Supplement):646.7'},{id:"B19",body:'Gilbert JS, Ryan MJ, LaMarca BB, Sedeek M, Murphy SR, Granger JP. Pathophysiology of hypertension during preeclampsia: Linking placental ischemia with endothelial dysfunction. American Journal of Physiology - Heart and Circulatory Physiology. 2008;294(2):H541-H550'},{id:"B20",body:'Granger JP, Alexander BT, Llinas MT, Bennett WA, Khalil RA. Pathophysiology of preeclampsia: Linking placental ischemia/hypoxia with microvascular dysfunction. Microcirculation. 2002;9(3):147-160'},{id:"B21",body:'Sanchez L, Prada CE, Riaño-Medina CE, Lopez M. Endothelial dysfunction and preeclampsia: Role of oxidative stress. Frontiers in Physiology. 2014;5:372'},{id:"B22",body:'Zárate A, Saucedo R, Valencia J, Manuel L, Hernández M. Early disturbed placental ischemia and hypoxia creates immune alteration and vascular disorder causing preeclampsia. Archives of Medical Research. 2014;45(7):519-524'},{id:"B23",body:'MacDonald JF, Xiong ZG, Jackson MF. Paradox of Ca2+ signaling, cell death and stroke. Trends in Neurosciences. 2006;29:75-81'},{id:"B24",body:'Executive summary. Neonatal encephalopathy and neurologic outcome, second edition. Report of the American College of Obstetricians and Gynecologists’ task force on neonatal encephalopathy. The Obstetrician and Gynaecologist. 2014;123:896-901'},{id:"B25",body:'O’Sullivan M. Leukoaraiosis. Practical Neurology. 2008;8:26-38'},{id:"B26",body:'Wassink G, Gunn ER, Drury PP, et al. The mechanisms and treatment of asphyxial encephalopathy. 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