The contribution of long-chain acyi carnitine to increase enzyme release during ischemia was investigated both in normal and diabetic rat hearts. 2-Tetradecylglycidic acid (TDGA) was used to inhibit acyl carnitine formation. Isolated working-heart preparations were perfused with glucose (11 mM) and palmitate (0.1 mM) in control and mild ischemie conditions. Ischemia induced lactate dehydrogenase (LDH) release from both normal and diabetic hearts, but the release was higher from the diabetics over a 15-min ischemie period. The ischemia-induced tissue accumulation of long-chain acyl carnitine also was greater in diabetic hearts compared with normal hearts. When TDGA was provided in the perfusate 10 min before the addition of palmitate, levels of acyl carnitine were significantly reduced (by ∼80%) in the ischemie tissue of both groups of hearts. Similarly, LDH release from ischemie hearts was markedly decreased in the presence of TDGA. A positive correlation was shown between LDH release over the ischemie period and the tissue levels of acyl carnitine at the end of ischemia. Significant improvement in mechanical function with TDGA was only observed in ischemie diabetic hearts. There was absolutely no difference in high-energy compounds under a given perfusion condition, either with or without TDGA, between normal and diabetic hearts. It is concluded that lessening the accumulation of fatty acid intermediates, such as acyl carnitine, may be important to prevent or to limit the loss of sarcolemmal integrity under ischemie conditions, especially in diabetic hearts.

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Copyright © 1986 by the American Diabetes Association
1986