Extracellular K+ accumulation during myocardial ischemia in isolated rabbit heart.

Abstract

Double-barreled valinomycin K+-sensitive electrodes were used to record extracellular K+ activity ([K+]o) in the isolated arterially perfused rabbit interventricular septum under conditions of global ischemia. During ischemia a triphasic pattern of [K+]o accumulation was observed consisting of an initial rise, a plateau phase, and a second rise. The initial rise (0.5-1 mM/min) was homogeneous throughout the preparation, reversible, and reproducible. It was augmented by increases in heart rate, contractility, and temperature. The level of the plateau phase (onset 12.3 +/- 3.1 min) was dependent on temperature and heart rate. Hyperkalemia, acidosis, or catecholamine release did not appear to be responsible for the plateau. The second rise in [K+]o (onset 24.2 +/- 4.6 min) was inhomogeneous and always associated with the development of rest tension and irreversible damage to the preparation. Cellular K+ influx mechanisms appeared to be at least partially intact throughout the plateau phase. K+ loss during ischemia could not be attributed to acidosis or catecholamine release, but substrate depletion may play a contributory role.