Ultrastructural and physiological changes induced by atractylate in the canine myocardium.
The myocardial cellular response to the cardiac glycoside atractylate, a known inhibitor of mitochondrial adenine nucleotide translocation, was examined physiologically, morphologically, and morphometrically in eight dogs. An isolated in situ segment of left ventricular tissue was employed in these experiments to eliminate collateral flow and the potential for large sampling error. It was found that atractylate infusion rapidly induced physiological and morphological changes suggestive of a loss of membrane regulation of ion flux in the arteriole, capillary endothelium, and myocardial cell. Also mitochondrial changes suggestive of adenine nucleotide translocase inhibition were observed. As these responses are similar to those induced by acute myocardial ischaemia, it is suggested that ischaemia and atractylate induce cell injury by similar mechanisms.
D000818:Animals; D001278:Atractyloside / Q000494:pharmacology*; D002199:Capillary Permeability / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000473:pathology; D004285:Dogs; D006027:Glycosides / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects*; D008929:Mitochondria, Heart / Q000648:ultrastructure; D009206:Myocardium / Q000648:ultrastructure*
D006027:Glycosides; D001278:Atractyloside