Effect of potassium-induced cardioplegia in hypothermia on myocardial energy, ammonium, and intermediary metabolism in man.

Cardiac muscle biopsy specimens were obtained from 33 patients undergoing open-heart surgery under K+-induced ischemic arrest in hypothermia (cardioplegic right atrial and right ventricular muscles) or under hypothermic ischemic arrest without K+-cardioplegia (noncardioplegia right atrial muscle), and sequential patterns of changes in the myocardial metabolism were studied by standard enzymatic techniques. The concentrations of the high energy phosphates were not only adequately preserved but actually exceeded the initial values in the cardioplegic muscles during the 40-min period of the ischemic arrest. In addition, elevated ammonia levels were neutralized by these muscles, and excessive variations in the myocardial intermediary metabolism were prevented. The levels of ATP were also adequately preserved by the noncardioplegic right atrial muscle during the 12-min period of ischemic arrest. But this protection was achieved at the expense of a 20% reduction in the myocardial creatine phosphate levels and other associated severe intracellular metabolic derangements. Changes in the myocardial intermediary metabolism, at the end of 12 min of ischemic arrest and at the end of 40 min of K+-cardioplegic arrest, were almost identical. The results of these studies suggest that, in contrast to the hypothermic arrest alone, K+-cardioplegia in hypothermia offers a superior myocardial metabolic preservation over an extended period of time.