Regional changes in intracellular potassium and sodium activity after healing of experimental myocardial infarction in cats.

After healing of experimental myocardial infarction in cat hearts, endocardial cells demonstrate persistent regional electrical changes. These include long action potential duration in surviving cells over the infarct scar, and short action potential duration and low membrane potential in border zone cells between the scar and normal tissue. We studied the basis for these electrophysiological changes by measuring intracellular potassium and sodium activity with ion-sensitive microelectrodes in normal, border, and infarct zone cells of the cat left ventricle 2-6 months after ligation of multiple distal tributaries of the left anterior descending and circumflex coronary arteries. In normal zone cells, intracellular potassium activity was 89.6 +/- 12.3 mM (mean +/- SD, n = 9), and sodium activity was 10.8 +/- 2.2 mM (n = 5). Neither was significantly different from infarct zone cells (91.2 +/- 15.0 and 10.5 +/- 3.0 mM, respectively). In contrast, border zone cells had significantly reduced intracellular potassium activity (71.4 +/- 5.1 mM, P less than 0.01, compared to normal and infarct zone cells) and increased intracellular sodium activity (19.1 +/- 5.9 mM, P less than 0.05, compared to normal and infarct zone cells). The membrane potential in border zone cells was more positive to calculated potassium equilibrium potential, and less sensitive to the change in the extracellular potassium concentration in the range between 2 and 10 mM, compared to normal and infarct zone cells.(ABSTRACT TRUNCATED AT 250 WORDS)