[Role of the sarcolemma in the morphogenesis of acute heart failure].
Acute heart insufficiency was simulated in dogs, rabbits and rats with experimental myocardial infarction, hypothyrosis, thyrotoxicosis, autoimmune cardiomyopathy, myocardium hypertrophy by exerting additional mechanical load on the heart (graded aortic stricture, swimming, running in a tread-ban). Irrespective of the basic pathological process the development of acute heart insufficiency was associated with generalized damage of plasmalemma of the majority of functioning cardiomyocytes, registered with colloid lanthanum. Plasmalemma damage precedes intracellular ultrastructural alterations and is reversible. Sarcolemma damages in non-functioning cardiomyocytes revealed in the focus of severe ischemia in experimental myocardial infarction is on the contrary indicative of irreversible cellular changes. The distinctions demonstrate that mechanisms causing damages in sarcolemma membrane can be different in conditions of preserved coronary blood flow and in severe ischemia.
D000818:Animals; D001327:Autoimmune Diseases / Q000150:complications; D006332:Cardiomegaly / Q000150:complications; D004195:Disease Models, Animal; D004285:Dogs; D006333:Heart Failure / Q000209:etiology / Q000473:pathology*; D006980:Hyperthyroidism / Q000150:complications; D008854:Microscopy, Electron; D009203:Myocardial Infarction / Q000150:complications; D009206:Myocardium / Q000648:ultrastructure*; D009230:Myxedema / Q000150:complications; D011817:Rabbits; D051381:Rats; D012508:Sarcolemma / Q000648:ultrastructure
Rol' sarkolemmy v morfogeneze ostroĭ serdechnoĭ nedostatochnosti.