Direct evidence that the hydroxyl radical plays a pathogenetic role in myocardial "stunning" in the conscious dog and demonstration that stunning can be markedly attenuated without subsequent adverse effects.
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Recent studies suggest that the hydroxyl radical (.OH) plays a pathogenetic role in postischemic ventricular dysfunction (myocardial stunning). This concept, however, is predicated exclusively on results obtained in anesthetized open-chest preparations, which are subject to the confounding influence of many unphysiological conditions and in which both myocardial stunning and free radical generation are greatly exaggerated. The lack of supporting evidence in more physiological animal models represents a major limitation of the .OH hypothesis of stunning. Furthermore, concern has been raised that myocardial stunning may be a period of rest necessary for full recovery, so that attenuation of the early phase of stunning by antioxidant therapy may have subsequent detrimental effects on the resting function and/or on the return of myocardial contractile reserve. To address these issues, in phase 1 of this study conscious unsedated dogs undergoing a 15-minute coronary artery occlusion received an intravenous...Keywords:
Stunning
Myocardial Stunning
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Recent studies suggest that oxygen-derived free radicals contribute to the pathogenesis of postischemic myocardial dysfunction (myocardial stunning). This concept, however, is predicated exclusively on results obtained in open-chest preparations, which are subject to the confounding influence of many unphysiological conditions. The lack of supporting evidence in more physiological animal models represents a major persisting limitation of the oxy-radical hypothesis of myocardial stunning. The goal of this study was to address two fundamental (and related) questions: 1) Does the open-chest animal model alter the phenomenon of myocardial stunning? 2) If so, how valid are the concepts, derived from such a model, regarding the pathogenetic role of oxy-radicals? In part 1 of the study, myocardial stunning after a 15-minute coronary occlusion was compared in 30 pentobarbital-anesthetized open-chest dogs and in 19 conscious dogs. For any given level of collateral flow during occlusion, the recovery of systolic ...
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Abstract Myocardial stunning can follow regional or global ischemia in the adult or immature heart. This report reviews some of our studies of the protean causes of stunning including energy and substrate depletion, inefficient oxygen utilization, calcium loading, acidosis, oxyradical damage, and summarizes studies and strategies to limit its occurrence. Data showing that reintroduction of molecular oxygen during reoxygenation of immature cyanotic hearts can cause stunning via a newly described biochemical pathway involving superoxide anion and nitric oxide are also included.
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Stunning
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Stunning
Myocardial Stunning
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Hibernating myocardium
Dobutamine
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Актуальность. Миокардиальный станнинг — феномен, заключающийся в продолжительном снижении сократительной способности миокарда после краткого периода ишемии/реперфузии, при котором не происходит омертвения ткани сердечной мышцы. Если изначально феномен станнинга ассоциировали исключительно с проявлениями ишемической болезни сердца, то в настоящее время имеется все больше свидетельств о том, что миокардиальный станнинг может осложнять совсем другую патологию. Цель: изучение результатов работ оте-чественных и зарубежных ученых, посвященных наблюдению феномена станнинга в медицине неотложных состояний, и систематизация накопленного клинического материала. Материалы и методы. Детальное изучение результатов современных клинических исследований, посвященных диагностике снижения сократительной способности миокарда у пациентов, находящихся в критических состояниях, которые развились не вследствие манифестации острого коронарного синдрома, обсуждению механизмов патогенеза миокардиальной дисфункции при этих состояниях и принципам оказания таким больным экстренной и специализированной медицинской помощи. Результаты. Для феномена миокардиального станнинга характерны следующие отличительные признаки: 1. Коронарный кровоток после перенесенного эпизода ишемии практически полностью восстанавливается. После ишемии очень часто регистрируется кратковременный период гиперперфузии. 2. Несмотря на восстановление коронарного кровотока, имеет место продолжительное снижение сократимости миокарда. 3. Необратимого повреждения кардиомиоцитов в период ишемии не происходит. 4. Снижение сократительной способности сердца, наблюдающееся после ишемии и последующей реперфузии, является полностью обратимым. Основными механизмами развития миокардиального станнинга являются: усиленная генерация активных форм кислорода в период реперфузии; перегрузка кардиомиоцитов кальцием; снижение сопряженности между процессами электрического возбуждения миокарда и его сократимостью. Продукция простациклина, активность ангиотензина I, II и ангиотензинпревращающего фермента, продукция брадикинина моделируют тяжесть мио-кардиальной дисфункции при станнинге. Причиной станнинга может быть индуцированная катехоламинами кардиотоксичность. Миокардиальный станнинг можно наблюдать у пациентов с геморрагическим, септическим шоком, субарахноидальными кровоизлияниями, на фоне проведения гемодиализа, после криза при феохромоцитоме, после реанимационной акции. Выводы. Миокардиальный станнинг требует своевременной диагностики, поскольку проведение гемодинамической коррекции не с помощью инотропной поддержки, а по другим направлениям, а именно за счет увеличения скорости объемной нагрузки (агрессивная инфузионная терапия) или применения вазопрессоров, может резко ухудшить состояние пациента вследствие увеличения нагрузки на ослабленное сердце.
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Hibernating myocardium
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Myocardial Stunning
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Abstract Myocardial stunning commonly occurs after cardiopulmonary bypass (CPB). Myocardial stunning can be cardioprotective under some conditions, but in other situations may actually contribute to myocardial infarction (MI). Vascular endothelial stunning may be one of the mechanisms by which myocardial stunning can cause MI. It has been found that 15 minutes of reversible ischemia is enough to cause elevations in vascular resistance and impairment of vasodilator responsiveness. However, no correlation between contractile dysfunction and microvascular stunning has been observed. Transduction defects (increased oxygen extraction and consumption despite normal regional oxygen blood flow and delivery) may be another mechanism by which stunning predisposes to MI, indicating uncoupling of substrate utilization from energy production. In addition, abnormalities in wall motion, oxygen free radical toxicity, hypotension, use of inotropic agents (leading to increased oxygen consumption, high heart rates, and arrhythmias) increase the risk of cellular necrosis. Following CPB, flow limitations due to diffuse atherosclerosis in some areas may result in poor contractility, and newly grafted areas have a high probability of becoming ischemic and stunned. These areas are likely to contribute to MI.
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The concept of myocardial stunning has been proposed by Braunwald and Kloner in early 1980's and is defined as transient postischemic myocardial dysfunction that persists after reperfusion, despite the absence of irreversible damage and restoration of normal or near normal coronary flow. Thus, the hallmark of stunned myocardium is the mismatch between coronary flow and myocardial function.The two most plausible hypotheses used to explain the pathogenetic mechanisms of myocardial stunning are calcium and oxyradical hypotheses. According to the first one, myocardial stunning is the result of impaired calcium homeostasis caused either by calcium overload or decreased responsiveness of myofilaments to calcium. The oxyradical hypothesis postulates that generation of free oxygen radicals depresses myocardial function after the ischemic episode. The exact mechanism is unknown, but it is probably due to extreme reactivity of oxyradicals that bind to some cellular components, impairing membrane permeability and function of various cell organelle. Stunned myocardium can be seen in numerous clinical situations in which myocardial ischemia has been followed by reperfusion. These include: coronary artery bypass surgery, acute myocardial infarction, stable, unstable and variant angina, percutaneous transluminal coronary angioplasty and cardiac transplantation.In majority of these situations, stunned myocardium is usually well tolerated. However, there is a group of high-risk patients in whom prolonged myocardial dysfunction due to stunning can cause serious hemodynamic instability, which requires pharmacological and/or mechanical support. Therefore, in order to avoid these situations, some authors have suggested that stunned myocardium should be prevented, rather than treated. Since stunned myocardium is by definition reperfused, with normal or near normal coronary flow, treatment is reserved only for those patients in whom stunned region is large enough to cause low cardiac output and hypotension. Revascularisation is usually unnecessary; however, there are situations in which episodes of repetitive stunning cause chronic myocardial dysfunction along with hibernated myocardium, when myocardial revascularization would be beneficial.
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