Новые аспекты в механизмах ишемического и реперфузионного повреждения миокарда

Introduction. The present article, in which a contemporary analysis of the literature on the pathophysiology of ischemic and reperfusion injury (IRI) of the myocardium is presented, focuses on the possible role played by of the calpain system and oxidative stress. Several process development options were proposed, including cytosolic and mitochondrial Ca2+ overload, reactive oxygen stress release, acute inflammatory response and metabolic degradation. The combined effect of all of the above factors produces irreversible ischemic and reperfused damage of cardiomyocytes.Materials and methods. The role of the calpain system in the creation of myocardial IRI was experimentally investigated. It was found that active calpain substrates play a significant role in the processes of cell cycle, apoptosis and differentiation, adversely affecting cardiomyocyte functionality. The calpain system is part of an integrated proteolytic system that is critical to the relationship between the structure and function of the cardiac sarcomere. Uncontrolled activation of calpain is indicated in the pathophysiology of many cardiovascular disorders. As shown by research, inhibitor calpain reduces the size of the zone of infarction following ischemia reperfusion and thus lessens the risk of “stunning” the myocardium. As is known, a consequence of IRI is acute myocardial infarction (AMI), which is a central factor in cardiovascular disease (CVD) and is one of the primary causes of mortality. Understanding the exact pathophysiological mechanisms remains an urgent problem for clinical physicians. To date, the mechanisms of IRI are not fully known, which creates certain difficulties in further treatment and prevention tactics. In addition, myocardial IRI is also an important issue for pathoanatomical service, since sudden coronary death can occur despite timely reperfusion therapy following AMI.Conclusion. The development of strategies for creating conditions that limit the degree of damage to myocardial tissues significantly increases the ability of the heart to withstand ischemic damage.Введение. В статье представлен современный анализ литературы относительно патофизиологии ишемического и реперфузионного повреждения (ИРП) миокарда, который сосредоточен на возможной роли кальпаиновой системы и окислительного стресса. Были предложены несколько вариантов развития процессов, включая цитозольный и митохондриальную Ca2+-перегрузку, выпуск реактивного кислородного стресса, острую воспалительную реакцию и ухудшение метаболизма. Совместное воздействие всего перечисленного производит необратимое ишемическое и реперфузированное повреждение кардиомиоцитов.Материалы и методы. Была экспериментально исследована роль кальпаиновой системы в создании миокардиального ИРП. Обнаружено, что субстраты активного кальпаина играют весомую роль в процессах клеточного цикла, апоптоза и дифференцирования, они отрицательно сказываются на функциях кардиомиоцитов. Кальпаиновая система — часть интегрированной протеолитической системы, которая является критической в отношениях между структурой и функцией кардиального саркомера. Бесконтрольная активация кальпаина вовлекает в патофизиологию множество сердечно-сосудистых нарушений. Ингибитор кальпаина, как показывали исследования, уменьшает риск «оглушения» миокарда и размер зоны инфаркта после ишемии реперфузии. Как известно, следствием ИРП является острый инфаркт миокарда (ОИМ), который занимает ведущую роль в сердечно-сосудистых заболеваниях (ССЗ), а также является одной из основных причин смертности населения. Понимание точных патофизиологических механизмов остается актуальной проблемой для клинических врачей. На сегодняшний день механизмы ИРП не полностью известны, что создает определенные трудности в дальнейшей тактике лечения и профилактике. Кроме того, миокардиальное ИРП является важным вопросом и для патологоанатомической службы, так как внезапная коронарная смерть может произойти несмотря на своевременную реперфузионную терапию после ОИМ.Заключение. Развитие стратегий по созданию условий, ограничивающих степень повреждения миокардиальных тканей, заметно увеличивает способность сердца выдерживать ишемическое повреждение

Role of epicardial adipose tissue in the development of cardiovascular diseases

Epicardial adipose tissue (EAT) has unique properties due to its special anatomical structure, thermoregulation, and metabolic activity. Dysregulated EAT provokes the synthesis of pro-inflammatory cytokines, disorders in the metabolism of fats and glucose, as well as contributes to fatty degeneration of the myocardium and heart failure development. EAT may serve as a risk factor and biomarker for cardiovascular diseases, and is also a potential therapeutic target. The purpose of this review was to highlight current research data on EAT, secreted adipokines, their effect on target tissue metabolism, and to systematize the relationship between EAT and cardiovascular diseases. In particular, its function, role in heart failure, atrial fibrillation, as well as the prognostic value of various microRNAs determined in EAT are highlighted

STUDYING THE STRUCTURE AND PROPERTIES OF METALLIC COMPOSITE MATERIALS

В работе исследована структура, морфология, микротвердость многослойных металлических композиционных материалов, механические свойства получаемых композитов и фрактограммы изломов. Показана возможность получения композиций из разных материалов методом сварки взрывом. Проанализированы возможные механизмы сцепления слоев.Structure, morphology, microhardness multilayer metal composite material, the mechanical properties of the resulting composites and fraktogrammy fractures studied in this work. The ability to obtain compositions of different materials by explosion welding is shown. Possible mechanisms of adhesion layers are analyzed.Работа выполнена при финансовой поддержке постановления № 211 Правительства Российской Федерации, контракт № 02.A03.21.0006 и НИР № 2014/236 на выполнение Госработ в сфере научной деятельности в рамках базовой части Госзадания № 2480 Минобрнауки РФ

Novel Aspects of Cardiac Ischemia and Reperfusion Injury Mechanisms

Introduction. The present article, in which a contemporary analysis of the literature on the pathophysiology of ischemic and reperfusion injury (IRI) of the myocardium is presented, focuses on the possible role played by of the calpain system and oxidative stress. Several process development options were proposed, including cytosolic and mitochondrial Ca2+ overload, reactive oxygen stress release, acute inflammatory response and metabolic degradation. The combined effect of all of the above factors produces irreversible ischemic and reperfused damage of cardiomyocytes.Materials and methods. The role of the calpain system in the creation of myocardial IRI was experimentally investigated. It was found that active calpain substrates play a significant role in the processes of cell cycle, apoptosis and differentiation, adversely affecting cardiomyocyte functionality. The calpain system is part of an integrated proteolytic system that is critical to the relationship between the structure and function of the cardiac sarcomere. Uncontrolled activation of calpain is indicated in the pathophysiology of many cardiovascular disorders. As shown by research, inhibitor calpain reduces the size of the zone of infarction following ischemia reperfusion and thus lessens the risk of “stunning” the myocardium. As is known, a consequence of IRI is acute myocardial infarction (AMI), which is a central factor in cardiovascular disease (CVD) and is one of the primary causes of mortality. Understanding the exact pathophysiological mechanisms remains an urgent problem for clinical physicians. To date, the mechanisms of IRI are not fully known, which creates certain difficulties in further treatment and prevention tactics. In addition, myocardial IRI is also an important issue for pathoanatomical service, since sudden coronary death can occur despite timely reperfusion therapy following AMI.Conclusion. The development of strategies for creating conditions that limit the degree of damage to myocardial tissues significantly increases the ability of the heart to withstand ischemic damage