Electrophysiologic effects and electrolyte changes in total myocardial ischemia.

Abstract

The ventricular membrane potential was measured in the perfused rabbit heart under control conditions and during total cardiac ischemia produced by an arrest of the coronary perfusion. The steady-state inactivation characteristic of the sodium system and the sodium dependence of the upstroke velocity were determined by measurements of the maximum rate of rise (Vmax) as a function of the resting potential (RP) and the [Na]0 to [Na]i ratio. The intracellular concentrations of sodium and potassium ([Na]i, [K]i) were estimated from measurements of the cellular electrolyte content, the total water content, and the volume of the extracellular space. Ischemia produced a net sodium gain of 58 mmol/kg dry weight and a slight loss of potassium. As a consequence, [Na]i increased and [K]i decreased. Under ischemia the resting potential was closer to the potassium equilibrium potential than in the controls. The changes in action potential configuration and plateau level suggested that ischemia inhibited the slow inward current. The Vmax decreased within 10 min of ischemia. Neither membrane depolarization nor a reduction in the sodium gradient could entirely explain the low Vmax of ischemic cells. It is concluded that the electrophysiologic effects of ischemia result from changes in ionic gradients and membrane electrical properties.