Electrical Properties and Conduction in Reperfused Papillary Muscle

Abstract

The reversibility of ischemia-induced changes of extracellular K + concentration ([K + ] o ), resting membrane potential (E M ), and passive cable-like properties, ie, extracellular resistance and cell-to-cell electrical coupling, and their relationship to recovery of conduction and contraction is described in 25 reperfused rabbit papillary muscles. No-flow ischemia caused extracellular K + accumulation, depolarization of E M , an increase in whole-tissue (r t ), external (r o ), and internal (r i ) longitudinal resistances, and failure of conduction and contraction. Muscles were reperfused 10 minutes after the onset of ischemia related cell-to-cell electrical uncoupling, ie, 26±1 minutes after arrest of perfusion. In 11 muscles, incomplete reflow occurred with only partial recovery of [K + ] o and r t . In the remaining 14 muscles, reperfusion caused a rapid and parallel decrease in [K + ] o , r t , and r o . When complete tissue reperfusion occurred, cell-to-cell electrical uncoupling was largely reversible. Thus, cell-to-cell electrical uncoupling did not indicate irreversible injury. Reperfusion induced a depolarizing current widening the difference between the K + equilibrium potential and the E M . This difference decreased after longer periods of reperfusion. Conduction was restored and conduction velocity approached preischemic values as cell-to-cell electrical interaction was reestablished and E M recovered. The recovery of r o preceded r i , decreasing the ratio of the extracellular to intracellular resistance early in reperfusion, an effect predicted to influence the amplitude of the extracellular voltage field and electrocardiographic ST segments during reperfusion.