TIME COURSE OF MYOCARDIAL HIGH-ENERGY PHOSPHATE DEGRADATION DURING POTASSIUM CARDIOPLEGIC ARREST

Abstract

Myocardial high-energy phosphate and glucose-6-phosphate levels were determined in the in vivo pig heart model during ischemic arrest and reperfusion to determine the effectiveness of K cardioplegia in myocardial protection. Pigs (35) were divided into 6 experimental groups consisting of 2 h normothermic arrest, 2 h hypothermic arrest, 2 h normothermic cardioplegic arrest and 1, 2 and 3 h hypothermic cardioplegic arrest. Myocardial biopsies from the left ventricle were obtained prior to arrest, every 30 min during the arrest interval and at 30 and 60 min of reperfusion. The measurement of ATP and creatine phosphate [CP] showed that cardioplegic arrest requires hypothermia to preserve high-energy phosphate levels in myocardial tissue; hypothermia, while not completely protective alone, is more effective than K caridoplegia alone in providing myocardial preservation during 2 h ischemic arrest; the combination of K cardioplegia and hypothermia is additive in providing an effective means of maintaining myocardial high-energy phosphate stores during 1, 2 and 3 h of ischemic arrest; myocardial reperfusion does not allow a return to preischemic ATP levels after 2 h of arrest, except following hypothermic cardioplegia; and extension of the duration of ischemic arrest to 3 h using hypothermic cardioplegia prevents recovery of high-energy phosphate stores to preischemic levels during reperfusion. Optimal preservation can be achieved during 2 h of ischemic arrest by using hypothermic K cardioplegia. The effects of myocardial reperfusion prevent full ATP and CP recovery following 3 h of arrest. No other technique studied was as effective in providing myocardial preservation.