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.