Electrical properties and conduction in reperfused papillary muscle

The reversibility of ischemia-induced changes of extracellular K+ concentra tion ([K+](o)), resting membrane potential (E-M), and passive cable-like pr operties, ie, extracellular resistance and cell-to-cell electrical coupling , and their relationship to recovery of conduction and contraction is descr ibed in 25 reperfused rabbit papillary muscles. No-flow ischemia caused ext racellular K+ accumulation, depolarization of E-M, an increase in whole-tis sue (r(t)), external (r(o)), and internal (r(i)) longitudinal resistances, and failure of conduction and contraction. Muscles were reperfused 10 minut es after the onset of ischemia related cell-to-cell electrical uncoupling, ie, 26 +/-1 minutes after arrest of perfusion. In 11 muscles, incomplete re flow occurred with only partial recovery of [K+](o) and r(t). In the remain ing 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 e lectrical uncoupling was largely reversible. Thus, cell-to-cell electrical uncoupling did not indicate irreversible injury, Reperfusion induced a depo larizing current widening the difference between the K+ equilibrium potenti al and the E-M. This difference decreased after longer periods of reperfusi on. Conduction was restored and conduction velocity approached preischemic values as cell-to-cell electrical interaction was reestablished and E-M rec overed. The recovery of r(o) preceded r(i), decreasing the ratio of the ext racellular to intracellular resistance early in reperfusion, an effect pred icted to influence the amplitude of the extracellular voltage field and ele ctrocardiographic ST segments during reperfusion.