A study on the electrophysiological heterogeneity of rabbit ventricular myocytes the effect of ischemia on action potentials and potassium currents.

With the whole-cell variant patch-clamp technique, action potentials (AP) and outward potassium currents of rabbit ventricular myocytes isolated from subendocardium and subepicardium were recorded and their changes were observed under normal and ischemia conditions. The results showed that (1) under normal condition, there were differences in the AP figures between ventricular subendocardial and subepicardial myocytes. Action potentials recorded from subepicardial myocytes had shorter action potential duration (APD) and a notch between phases 1 and 2, compared with those of subendocardial myocytes. The resting potential had no significant difference between these two populations of the action myocytes; (2) under ischemia condition, the notch of action potentials of subepicardial myocytes disappeared and the APD was shortened even more, compared with that of subendocardial myocytes; (3) under normal condition, the density of steady-state outward potassium currents of subepicardial myocytes was significantly greater than that of subendocardial myocytes; (4) under ischemia condition, the increase of steady-state outward potassium currents of subepicardial myocytes was greater than that of subendocardial myocytes. Glybenclamide could partly reverse the above changes. It is suggested that the increase of steady-state outward potassium currents during ischemia is mainly due to the opening of I(K-ATP) channels as a result of the deficiency of intracellular ATP caused by ischemia.