Acyl-CoA inhibition of adenine nucleotide translocation in ischemic myocardium.
The translocation of adenine nucleotides across the inner mitochondrial membrane and the tissue concentration of long-chain acyl-CoA esters were studied in dog heart after experimental myocardial ischemia. Ligation of the anterior coronary artery initiated events leading to an early decrease in adenine nucleotide translocase activity. A reciprocal increase in the concentration of heart tissue long-chain acyl-CoA esters was also observed. Adjacent nonischemic tissue showed changes intermediate between that of ischemic and normal heart tissue. It is postulated that a decrease in fatty acid oxidation after myocardial ischemia would lead to an accumulation of long-chain acyl-CoA esters, which in turn would inhibit adenine nucleotide translocation. The net result would be a lowering of the energy charge of the cell, adversely affecting muscle contraction and electrical conduction.
D000105:Acetyl Coenzyme A / Q000378:metabolism* / Q000494:pharmacology; D000227:Adenine Nucleotides / Q000378:metabolism*; D000818:Animals; D003065:Coenzyme A / Q000031:analogs & derivatives*; D003326:Coronary Circulation; D004285:Dogs; D007511:Ischemia / Q000378:metabolism; D008566:Membranes / Q000378:metabolism; D008931:Mitochondria, Muscle / Q000378:metabolism; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D009713:Nucleotidyltransferases / Q000378:metabolism; D010101:Oxygen Consumption
D000227:Adenine Nucleotides; D000105:Acetyl Coenzyme A; D009713:Nucleotidyltransferases; D003065:Coenzyme A