Energy metabolism has a strong influence on the electrical activities of cardiac muscle (Trautwein et al., 1954; De Mello, 1959; MacLeod and Daniel, 1965; for review see Carmeliet, 1978). When cardiac muscle is exposed to anoxic conditions or metabolic inhibitors, or is depleted of substrates, the plateau of the action potential is depressed in the early stage of the metabolic impairment. If the metabolic depression is continued, the electrochemical gradient for ions is decreased and thereby the maximum rate of rise, the overshoot of the action potential, and the resting membrane potential are reduced (Kohlhardt and Kubier, 1975; Nargeot, 1976; Nargeot et al., 1978; Payet et al., 1978). The primary effect of metabolic depression is a decrease of high-energy phosphate, such as ATP and phosphocreatine. A recent study using nuclear magnetic resonance showed a rapid reduction of phosphocreatine to about 15% of the control and of ATP to about 90% within 5–10 min when the rate of oxidative phosphorylation was prevented either by replacement of O2 with N2 or by addition of cyanide (Allen et al., 1985). If the supplementary action of the glycolysis was also reduced, the ATP level was reduced more markedly to about half of the control.