Reperfusion-induced accumulation of long-chain acylcarnitines in previously ischemic myocardium.

Long-chain acylcarnitines (LCA) have been shown to accumulate during myocardial ischemia and to contribute to malignant derangements characteristic of ischemia. We detail the time course of the increase in LCA levels during both ischemia and reperfusion. Evidence indicates an additional specific reperfusion-induced increase in LCA that peaks at 2 min and decreases to basal levels by 30 min. This increase in LCA during reperfusion is observed after 2-, 10-, or 20-min ischemia and is inhibited by the presence of the carnitine palmitoyl transferase 1 (CPT1) inhibitor phenyloxirane carboxylic acid (POCA). A role for increased LCA in mediating "reperfusion damage" is not indicated, however, because POCA did not attenuate either the incidence of ventricular fibrillation (VF) during early reperfusion or the survival rate of rats undergoing 24-h reperfusion after 10-min occlusion.