THE ENERGETICS OF THE QUIESCENT HEART-MUSCLE - HIGH POTASSIUM CARDIOPLEGIC SOLUTION AND THE INFLUENCE OF CALCIUM AND HYPOXIA ON THE RAT-HEART

Heart basal metabolism has been classically studied as the energy expe nditure of those processes unrelated to mechanical activity and often measured by rendering the heart inactive using cardioplegic solutions (usually by increasing extracellular K concentration ([K](e)). In arte rially perfused rat heart (at 25 degrees C), raising [K]e from 7 to 25 mM at a constant extracellular Ca concentration ([Ca](e)) (0.5 mM), i nduced an increase in resting heat production (Hr) from 4.1 +/- 0.3 to 5.1 +/- 0.3 mol. wt g(-1). Under 25 mM K additional increase in [Ca]( e) further increased Hr to 6.0 +/- 0.4, 7.0 +/- 0.4 and 8.3 +/- 0.9 mo l. wt g(-1) for 1, 2 and 4 mM Ca, respectively. While under 7 mM K per fusion Hr was not affected by 4 mu M verapamil, under 25 mM K and 2 mM Ca 0.4 mu M verapamil induced a decrease in Hr (-1.6 +/- 0.2 mol. wt g(-1), n = 5, P < 0.001). Caffeine increased Hr under 0.5 mM Ca and 7 mM K perfusion (+0.32 +/- 0.06 and +1.19 +/- 0.25 mol. wt g(-1) for 1 and 5 mM caffeine respectively), but under 25 mM K conditions Hr was n ot affected by caffeine 2 mM. Severe hypoxia decreased Hr under both 7 and 25 mM K (3.7 +/- 0.5 to 2.7 +/- 0.4 mol. wt g(-1) and 7.0 +/- 0.4 to 2.2 +/- 0.5 mol. wt g(-1) respectively) suggesting that the increa sed Hr associated with the verapamil sensitive fraction of heat releas ed is associated to a mitochondrial mechanism. Therefore, the use of h igh [K](e) overestimates basal values by increasing a verapamil sensit ive fraction of the energy released. In addition, high [K](e) modifies a caffeine sensitive energy component probably due to a depletion of caffeine-dependent Ca stores.