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American Journal of Pathology, Vol 131, 5-11, Copyright © 1988 by American Society for Investigative Pathology

REGULAR ARTICLES

Transmural differences in the postischemic recovery of cardiac energy metabolism

SM Humphrey, MA Vanderwee and JB Gavin
Department of Pathology, University of Auckland School of Medicine, New Zealand.

After 25 minutes of ischemia, in the isolated rat preparation, hearts fail to reestablish adequate contractile function. To determine whether this failure was associated with a transmural variation in the metabolic response of myocardial cells to reperfusion, the authors subjected hearts to 25 minutes of global ischemia with and without 5 or 20 minutes of reperfusion. After freeze-drying the left ventricular myocardium was divided into subepicardial (EPI) and subendocardial (ENDO) regions before estimating the lactate, total adenine pool metabolites, and creatine phosphate (CP) and phosphate concentrations in each region. Other groups of hearts were perfusion-fixed with glutaraldehyde then injected with nuclear track emulsion to demonstrate that a high proportion of capillaries in both the subendocardial (89%) and subepicardial (95%) myocardium transmitted perfusate after 5 minutes of reperfusion. Reperfusion removed lactate equally from each region. Thus the differences in the capacity of reperfusion of these regions to recover CP (ENDO, 100%; EPI, 168% of preischemic values), to elevate adenosine triphosphate (ATP) (ENDO, 32%; EPI, 63%), or to retain adenosine monophosphate (AMP) (ENDO, 625%; EPI, 277%) were unlikely to be due to regional differences in microvascular function. Despite the better preservation of both structure and metabolism in the subepicardium, there was, during reperfusion, a progressive loss of purine precursors from cells in both regions of the myocardium. These results suggest that the loss of ability of the myocardium to recover significant function after relatively short periods of ischemia is due to their inability, on reperfusion, to synthesise sufficient ATP from the available precursors. This capacity for resynthesis of ATP is lost more rapidly in the subendocardial than in the subepicardial myocardium.