[Role of myocardial hypoxic lesions in the development of heart failure in the presence of pancreonecrosis].
Experimental pancreonecrosis was simulated in 50 Wistar rats. Following 24 hours, the mechanisms of cardiac lesion were revealed, by applying a model of the perfusion isolated heart by the method described by Fallen et al. and by estimating the force and velocity parameters of cardiac contractility. Activation of free radical processes and hypoxia were ascertained to be the most important pathogenetic factors of pancreatogenic heart failure, which was substantiated by the results of the investigations on rats that had received the energy-rich agent reamberin in a dose of 10 mg/kg before simulation of pancreonecrosis.
Ershov
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D000818:Animals; D005609:Free Radicals / Q000378:metabolism; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000209:etiology / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D019283:Pancreatitis, Acute Necrotizing / Q000150:complications / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar
D005609:Free Radicals