METABOLIC INHIBITION induced by hypoxia or by pharmacological agents is accompanied by pronounced changes in the electrical activity of the heart. In contractile myocardial fibers, the first and most pronounced effect of hypoxia is a shortening of the action potential (Fig. 1 A); later the resting potential, as well as the amplitude of the action potential, is reduced and conduction is impaired.'" 1 The effects are frequency dependent.'12 In Purkinje fibers, the effects of hypoxia are less pronounced and depend on the external K+ concentration. At low external K+(2.7 mM), hypoxia results in a prolongation of the action potential; secondary slow depolarizations may interrupt the repolarization process (Fig. IB) and repolarization may fail completely, resulting in a depolarization to the plateau level, with or without oscillatory behavior.'At 5.4 miu [K+] o, the disturbances of the repolarization process are less pronounced or absent and, after prolonged hypoxia, the action potential shortens (Fig. 1C).

Metabolic inhibition by dinitrophenol (DNP), monoiodoacetate (MIA), azide, and cyanide causes changes similar to those observed during hypoxia. 5 In general, the shortening of the action potential is most pronounced with MIA. Dinitrophenol at a low concentration (2 x 10~(i M), on the other hand, may prolong the action potential in the frog ventricle" and in sheep Purkinje fibers (Fig. 2, A and B).