The Role of Beta-Adrenoceptors in Ischemia-Induced Acidosis in the Isolated Rat Heart : A 31-P NMR Study

It has been known for a long time that ischemia of the heart results in a decrease of the tissue pH (1,2,3). Since glycolysis and glycogenolysis are accelerated during the initial phase of ischemia (3,4,5,6), it is reasonable to assume that a correlation exists between these processes and acidification (7,8). On the basis of this assumption, experimental protocols have been devised to examine whether myocardial beta-adrenergic receptor stimulation plays a part in the medhanism of ischemia-induced intracellular acidification. Studies performed on the dog heart “in situ” have shown that administration of beta-adrenergic blocking drugis results in a reduction of the acidosis induced by temporary coronary occlusion (9,10,11,12). Using 31-P NMR speotroscopy it has also been demonstrated that propranolol is capable of reducing the degree of acidosis developed during total ischemia of the isolated rat heart (13,14). However, the use of beta-adrenergic blocking agents possessing subsidary properties has revealed that the action of these drugs on intracellular couldl also be partly mediated by the membrane-stabilizing property certain of them possess (9,10,14,15).