Resting membrane potential, extracellular potassium activity, and intracellular sodium activity during acute global ischemia in isolated perfused guinea pig hearts.

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Abstract
Transmembrane potentials, extracellular potassium activity, and intracellular sodium activity were determined during acute global ischemia in Langendorff perfused guinea pig ventricles by microelectrode techniques. Resting membrane potential decreased with a sigmoidal time course from -82 mV to -49.5 +/- 2.7 mV (SD, n = 6) and extracellular potassium activity increased from 4 to 5 mM to 14.7 +/- 1.3 mM (n = 8) during 15 minutes of ischemia. The estimated potassium equilibrium potential was 7 mV more negative than resting membrane potential prior to occlusion, but approached resting membrane potential during ischemia. An increase in extracellular potassium accumulation occurred when heart rate was increased abruptly from 60 to 170 beats/min. After rapid stimulation, a transient decrease of extracellular potassium activity occurred which was abolished in the presence of 10(-6) M strophanthidin. If the preparations were paced before and after aortic occlusion at a constant rate, potassium accumulation was independent of heart rate within a range of 50-170 beats/min. Intracellular sodium activity was 8.8 +/- 2.8 mM (n = 8) prior to occlusion and decreased slightly to values between 4.7 and 7.6 mM after 10-15 minutes of ischemia. The results suggest that relative potassium permeability largely predominates over relative sodium permeability during the decrease of resting membrane potential after interruption of aortic flow. Furthermore, active sodium-potassium exchange compensates for the rate-dependent fraction of potassium efflux and maintains a low intracellular sodium activity. For reasons of electroneutrality, the potassium efflux underlying extracellular potassium accumulation must be balanced by an equivalent charge movement which is not carried by sodium. The most probable hypothesis regarding the charge carriers is that net potassium efflux occurs secondary to efflux of phosphate and lactate generated during ischemia.