Metabolic and physiological differences between zero-flow and low-flow myocardial ischemia: effects of L-acetylcarnitine |
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Authors: | Dennis J. Paulson Ph. D. Mary J. Schmidt Jeff Romens Austin L. Shug Ph. D. |
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Affiliation: | (1) Present address: Metabolic Research Laboratory, William S. Middleton Memorial Veterans Hospital, 2500 Overlook Terrace, 53705 Madison, Wisconsin, USA;(2) Department of Neurology, University of Wisconsin-Madison, Madison, WI, USA |
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Abstract: | Summary The metabolic and physiologic differences between low-flow and zero-flow ischemia of varying duration were compared in the isolated perfused rat heart. Hearts subjected to 60 and 90 minutes of zero-flow ischemia recovered less cardiac work than hearts subjected to low-flow ischemia. Low-flow ischemia caused a build-up of both myocardial long-chain acyl coenzyme A and acyl carnitine esters, while zero-flow ischemia produced no change in long-chain acyl carnitine and only a transient increase in long-chain acyl coenzyme A. High energy phosphate depletion was greater in zero-flow ischemia. Perfusion with excess free fatty acids decreased the recovery of cardiac work after low-flow ischemia but had no effect after repeated episodes of zero-flow ischemia. L-Acetylcarnitine improved the recovery of cardiac work after low-flow ischemia in hearts perfused with 0.4 and 1.2 mM palmitate. With zero-flow ischemia, L-acetylcarnitine had no effect on the recovery of cardiac work in hearts perfused with 0.4 mM palmitate and a slight but statistically significant effect with 1.2 mM palmitate. Possible protective mechanisms of L-acetylcarnitine against ischemic damage are discussed. |
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Keywords: | carnitine perfused rat heart long-chain acyl coenzyme A |
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