[Cardiac damage and protection in acute fatal blood loss].
Experiments on dogs and albino non-inbred male rats undergone a 4-5-min clinical death under the conditions of the whole organism and isolated isovolumetric contracting heart revealed phasic systemic hemodynamic and myocardial contractile disorders. The leading pathogenetic factors of postresuscitational cardiac damage are excessive catecholamine stimulation of cardiac beta-adrenoreceptors, impaired energy metabolism, excessive activation of free radical processes, metabolic acidosis, secondary hypoxia, and endogenous toxemia. The heart was found to be at the most damaged within the first hour after resuscitation. The use of antihypoxants, antioxidants, beta-adrenoblockers and Ca-channel blockers were pathogenetically substantiated to diminish postresuscitational cardiac damages.
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D000818:Animals; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D006333:Heart Failure / Q000209:etiology / Q000503:physiopathology*; D006439:Hemodynamics; D006470:Hemorrhage / Q000150:complications / Q000503:physiopathology*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D051381:Rats; D012151:Resuscitation / Q000009:adverse effects*