Absence of a relationship between extracellular potassium accumulation and contractile failure in the ischemic or hypoxic rabbit heart.

Ischemia and hypoxia both cause a rapid loss of potassium from myocardial cells. We have investigated the relationship between the accumulation of potassium in the extracellular fluid and the early loss of contractility. Experiments were performed on the isolated rabbit heart perfused with physiological saline at 36 degrees C, paced at 3 Hz. Tension was recorded from the apex. Extracellular potassium concentration [( K+]o) was recorded with small ion-selective electrodes. After the onset of global ischemia, [K+]o rose within 15 sec and reached 9.5 +/- 1.1 mmoles/liter after 5 min. Developed tension (T) fell to 9 +/- 2% of control over the same period. During substrate-free hypoxia, T declined at a similar rate, and [K+]o rose slowly to 5.5 +/- 0.1 mmoles/liter after 5 min. The relationship between [K]o and T during normal perfusion and oxygenation was investigated by incrementally increasing the perfusate [K+]. T dropped to 78.6 +/- 4.5% of control at a [K+]o of 9 mmoles/liter. Comparison of the relationship between [K+]o and T during high-potassium perfusion, ischemia, and hypoxia shows that extracellular potassium accumulation per se makes almost no contribution to the decline of contractile function in ischemia or hypoxia. (Values are means +/- S.E., N = 5.)