ACCORDING to functional,1-3 biochemical,4-9 and clinical,10-12 data and histological13-22 evidence, the use of citrate salts in inducing cardiac arrest causes myocardial damage which correlates with functional disorders of the heart during the postarrested period. Due to the binding by the citrate ion of bivalent cations, particularly of calcium, muscular function is paralyzed and myocardial edema occurs as a consequence of the abolished stability of the cellular membrane.
At present, chemical arrest has been abandoned and cardioplegia in open heart surgery is accomplished by either selective cardiac hypothermia or electrically induced cardiac standstill. A number of experimental studies and open heart operations2,23-27 have demonstrated the relatively great safety of these two procedures as opposed to normothermic ischemic or chemical arrest. However, there still remains the question, if not even greater protection might be achieved by suitable drugs. In any type of cardiac arrest, the membrane of