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Am J Physiol 228: 689-692, 1975;
0002-9513/75 $5.00
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American Journal of Physiology, Vol 228, Issue 3, 689-692
Copyright © 1975 by American Physiological Society

ARTICLES

Acyl-CoA inhibition of adenine nucleotide translocation in ischemic myocardium

AL Shug, E Shrago, N Bittar, JD Folts, and Koke JR

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.


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