The biology of the myocardium in chronic hypoxia. Note I. Myocardial lesions in experimental chronic heart failure.
The biology of the myocardium was studied in chronic heart failure, especially in the course of compensatory hypertrophy induced experimentally by partial stenosis of the aorta for 10 months and the administration of large isoproterenol doses for 7 months. In the stage of acute aggression, varied disseminated ultrastructural lesions are predominant, with the decrease of energy reserves, hydroelectrolytic and ECG perturbations. In the stage of ultrastructural compensatory hypertrophy, there is a prevalence of normal myocytes or others presenting regenerative aspects next to progressive fibrosis reflected biochemically by return to almost normal values, with certain oscillations due to the presence of some lesional foci, also recorded on the ECG tracings. The question of the pathogenesis and prognosis of these lesions is discussed.
D000818:Animals; D001012:Aorta, Abdominal; D001024:Aortic Valve Stenosis / Q000209:etiology / Q000473:pathology; D002908:Chronic Disease; D004195:Disease Models, Animal; D004562:Electrocardiography; D005260:Female; D006168:Guinea Pigs; D006333:Heart Failure / Q000209:etiology / Q000473:pathology*; D000860:Hypoxia / Q000209:etiology / Q000473:pathology*; D007545:Isoproterenol / Q000633:toxicity; D008026:Ligation; D008297:Male; D008854:Microscopy, Electron; D009206:Myocardium / Q000648:ultrastructure*; D051381:Rats; D011919:Rats, Inbred Strains
D007545:Isoproterenol