Sequential analysis of altered myocardial metabolism and contractility induced by normothermic arrest and reperfusion

Abstract

Normothermic anoxic arrest by aortic cross clamping, a widely used clinical technique, is associated with metabolic changes in the myocardium which are incompletely understood. Using the isovolumetric balloon model and “stop-freeze” biopsy technique, a study of myocardial contractility and metabolism was performed in 29 intact dogs supported by cardiopulmonary bypass and subjected to 60 min of normothermic anoxic arrest, followed by 30 min of reperfusion. A marked reduction in total high energy phosphates (62%), glycogen (63%), and an increase in lactate production (243%) denote a shift to anerobic metabolism during the period of arrest. Despite 30 min of reperfusion, total high energy nucleotides remained depressed ( P < 0.001). Nevertheless, intermediary metabolic recovery and a reversion to aerobic metabolism was evidenced by falling lactate levels (53%), rising glycogen (51%), and increasing creatine phosphate (1100%). These data suggest that persistent abnormal myocardial carbohydrate metabolism and low levels of high energy nucleotides prevent contractile recovery following normothermic anoxic arrest and reperfusion. While creatine appears to be preserved for the energy pool, the increase in creatine phosphate does not appear to be adequate to overcome depression of the nucleotides.