Abstract
In multicellular preparations, there are differences in action potential configuration between endocardium and epicardium, and electrophysiological alterations induced by ischemia are more drastic in epicardium than in endocardium. The present study was designed to examine electrophysiological properties of single cardiac myocytes enzymatically isolated from the endocardial and epicardial surfaces of the cat left ventricle and to determine whether the differential responses to ischemia of intact tissue occur in single cells. Action potentials recorded from the isolated single cells of epicardial surface had lower action potential amplitude and a prominent notch between phase 1 and phase 2, compared with those of the cells isolated from the endocardial surface; these findings are similar to those in intact endocardial and epicardial preparations. Resting membrane potentials recorded from both endocardial and epicardial single cells were sensitive to the change in extracellular K concentration and had properties of a K electrode. Action potential duration was frequency dependent in both cell types and was shorter in epicardial cells than in endocardial cells at a stimulation rate of 3 Hz. When the cells were superfused with Tyrodeʼs solution that was altered to mimic an ischemic environment in vivo (Po2, 30–40 mm Hg; pH 6.8; [K], 10 mM; and glucose free), resting membrane potential, action potential amplitude, and action potential duration were reduced, and the refractory period was shortened in both endocardial and epicardial single cells, but there were no differences in the degree of changes in action potentials and refractory periods induced between the two cell types. Action potential changes induced by L-a-lysophosphatidylcholine (5–40 mg/l) were also similar in endocardial and epicardial single cells. These results lead us to suggest that the differences in action potential configuration between endocardial and epicardial cells are due to intrinsic electrophysiological properties but that their different responses to ischemia in intact cardiac tissues may be due to the extracellular and electrotonic influences of the neighboring cells.
