Abstract
Administration of acetaldehyde to rats by inhalation or intraperitoneally (in repeated doses) provokes an emergence of micronecroses in the myocardium. Administration of acetaldehyde in a dose causing no injury to the myocytes potentiates the cardionecrotic action of adrenalin. Pretreatment with L-DOPA potentiates while that of L-alpha-methyl-DOPA or alpha-methyl-p-tyrosine averts the necrosogenous action of acetaldehyde. Under isolated heart perfusion, acetaldehyde administered in the concentrations that exceeded 2-fold and more those in the blood in experiments in vivo had no necrosogenous action. The degree of the adrenalin-induced lesions of the isolated myocardium remained unchanged in the presence of acetaldehyde. It is assumed that the cardionecrotic effect of acetaldehyde is mediated by catecholamines and is effected by stimulation of biogenic amine release from neurons and chromaffin tissue, and is not linked with direct acetaldehyde effect on the realization of the alterative action of catecholamines.
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