Electrophysiological and inotropic effects of Coenzyme Q10 on guinea pig ventricular muscle depolarized by potassium under hypoxia.

The electrophysiological and inotropic effects of Coenzyme Q10 (CoQ10) on isoproterenol or barium-induced slow responses in ventricular papillary muscle, depolarized by high K+ concentration (21.6 mM) under hypoxia (PO2 = 40 mmHg), were studied with microelectrode techniques. For the isoproterenol-induced slow response, application of CoQ10 (50 micrograms/ml), which was emulsified with the aid of a special solvent, increased the maximum rate of rise of action potentials (Vmax), an indicator of the slow inward current, by about 40%, with no consistent effect on the action potential duration and developed tension. Application of the solvent alone produced a significant decrease in both Vmax and developed tension. However, in these solvent-pretreated preparations, CoQ10 produced a significant (by about 50%) recovery in both Vmax and developed tension. The action potential duration was not changed by either the solvent alone or the application of CoQ10. The developed tension of the slow response consisted of early and late components. CoQ10 produced significantly more recovery in the late component than in the early one, suggesting that the recovery effect was due to increased slow inward Ca2+ current. CoQ10 did not reverse any parameter in the slow response induced by BaCl2 (0.2 mM). The results suggest that CoQ10 has significant but limited reversing effects on the hypoxia-induced deterioration of the slow response, and that the recovery is presumably due to increased availability of slow channels via increased production of ATP.