Pathogenesis of isoproterenol-induced lesions in the rat myocardium.
The aim of this study was to investigate the action of isoproterenol (ISP) on the myocardium by means of light microscopy, histochemistry, autoradiography with tritiated ISP and electron microscopy. One hundred and sixty four Wistar rats were divided into 8 groups. Group A, B, C and D were given 10 mg/kg i.p. ISP (plus 5 uC of tritiated ISP). The animals were sacrificed at different intervals. Group E served as control to proceeding groups. Group F was given 10 mg/kg i.p. ISP and subjected to "holding" stress; Group G was its corresponding control. Group H received 9 mg/kg. prenylamine, as inhibiting drug, 1 hour before and hour after ISP injection. Histopathology of "infarct like" lesions presenting localized necrosis, myocytolysis, homogenization and positive tests for ischemia are correlated to the localization of tritiated ISP on sarcolemma and to changes in succine dehydrogenase enzymes in the groups A, B, C and D. Hypercontraction and widening of Z bands of sarcomers are found in electron microscopy. These ischemic changes are inhibited by prenylamine, a drug acting as moderator of catecholamine effects by slowing down Ca transport. It is concluded that myocardial necrosis induced by ISP is probably due to an increased activation of the "calcium pump". The ISP provoked lesions appear to be a promising model to study experimental myocardial necrosis.
D000818:Animals; D006321:Heart / Q000187:drug effects*; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology / Q000633:toxicity*; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000473:pathology; D051381:Rats
D007545:Isoproterenol