Effect Of Ischemia On Slowly Activating Delayed Rectifier K～+ Current Of M Cell

Objective: Electrophysiological heterogeneity was observed within ventricle. A unique population of cells (M cells) exists in the midmyocardial layers of ventricle. The hallmark of the M cell: prominent spike-dome morphology of action potentials; the maximal rate of rise of the action potential upstroke; prominent phase 1 repolarization; prolongation of APD and more pronounced APD-rate relationship; decrease of the rest membrane potential. The primarily ionic basis for its electrophysiological characteristics of the M cells is a weaker Iks. Iks is the main outward current contribution to action potential repolarization. It shows a nearly relationship between abnormal Iks current and arrhythmia. In this article, I will study the effect of ischemia on Iks current of cardiac myocytes.Methods: The whole cell recording patch clamp technique was used to investigate the Iks tail current density of enzymatic isolated M cell, sub-endocardial and sub-epicardial myocytes. Different bath solution component was used to simulate the normal and ischemic status and Iks tail current was measured under each status.Results: Iks current was significantly smaller in M cell than in sub-endocardial myocytes or sub-epicardial under normal status. Iks current of all three layers myocytes was significantly smaller under ischemic status?3 ?than that under normal status. But the decrease of three layers myocytes is not in equal extent, the decrease of M cell was significantly greater than that of sub-endocardial myocytes and sub-epicardial.Conclutions: Under ischemic condition, the decrease of Iks could prolong the mid-late repolarization phase of APD. It could cause BAD and then arouse TdP. Because the decrease of M cell was significantly greater than that of sub-endocardial myocytes and sub-epicardial myocytes, it could increase TDR. Cardiac arrhythmias could last due to reentrance that secondary the increase of TDR. So, to increase Iks current is a good idea to control the occurring and development of cardiac arrhythmias.