Fatty acylcarnitine accumulation and membrane injury in ischemic canine myocardium.

Although previous work has shown that long chain fatty acylcarnitine derivatives accumulate in ischemic canine myocardium, their role in the production of irreversible injury and associated sarcolemmal membrane injury is undefined. The present study examines the temporal and topographic relationship of the accumulation of long chain acylcarnitine with the uptake of technetium pyrophosphate and tissue calcium content during ligation of the left anterior descending coronary artery (LAD) in canine myocardium. After 60 minutes of fixed LAD ligation, there was no significant increase in long chain acylcarnitine content in the ischemic subendocardium compared with the corresponding nonischemic value. However, the ischemic subendocardium was irreversibly injured at this time, as assessed by a 4-fold increase in tissue calcium content and a 20-fold increase in technetium-99m pyrophosphate uptake after reperfusion. The ischemic subepicardium showed a 41% increase in long chain acylcarnitine content compared with the corresponding nonischemic subepicardium. However, the ischemic subepicardium contained only 50% of the calcium content and 10% of the technetium-99m pyrophosphate uptake found in the ischemic subendocardium. It is concluded that increases in fatty acylcarnitine can be dissociated from the development of irreversible ischemic injury during fixed LAD occlusion in ischemic canine myocardium.