模拟失重4周大鼠心肌细胞动作电位的改变及其离子机理

Changes of action potentials of cardiac myocytes from 4 wk tail suspended rats and its related ionic mechanisms

目的 观察模拟失重 4周大鼠心肌细胞动作电位 (AP)的改变 ,并进一步阐明其离子机理。 方法 采用尾部悬吊大鼠模型模拟失重 ,胶原酶分离心肌细胞 ,用膜片钳全细胞方式记录单个心肌细胞的膜电容、AP、跨膜内向钙电流 (ICa)和瞬时外向钾电流 (Ito)等。 结果 正常对照大鼠左室游离壁心肌细胞的动作电位时程 (APD)较心尖部位的长 (P<0 .0 5 ) ;悬吊组大鼠左室游离壁心肌细胞 APD2 0 较对照组缩短有显著性意义 (P<0 .0 1) ,而在心尖部位则无此改变 ;在对照组 ,左室游离壁细胞的 ICa密度 (AP复极化 2 0 %即时电位水平时记录 )大于心尖部位 (P<0 .0 5 ) ;在左室游离壁部位 ,悬吊组的 ICa密度小于对照组 (P<0 .0 5 )。 结论 正常大鼠左室不同部位心肌细胞的 APD是非均一的 ;模拟失重 4周可引起大鼠心肌细胞 APD2 0 改变 ,且具有部位的差异 ;复极化 2 0 %即时电位水平的ICa不同或改变是引起正常心肌细胞 APD部位非均一性和模拟失重后左室游离壁心肌细胞 APD2 0

Objective To observe the changes of action potentials (AP) of cardiac myocytes from 4 wk tail suspended rats, and elucidate its related ionic mechanisms. Methods Cardiac myocytes were isolated from suspended and control rats with collagenase. Using whole cell recording mode of patch clamp technique, membrane capacitances, AP, calcium currents (I Ca ) and transient outward currents (I to ) were recorded from a number of single ventricular myocyte. Results In control rats, the action potential duration (APD) of cardiac myocytes from left ventricular free wall (FW) was longer than that from apex ( P <0.05). The APD 20 of cardiac myocytes from FW in suspended rats was shorter than that in control rats ( P <0.01), but there was no obvious change in apex myocytes. In control rats, I Ca density (measured at an instant potential of 20% AP repolarization) of cardiac myocytes from FW was greater than that from apex ( P <0.05). The I Ca density of suspended rats was smaller than that of control rats in the region of FW. Conclusions There is a regional heterogeneity of APD of cardiac myocytes in left ventricle of normal rats. Four wk simulated weightlessness may lead to an alteration in APD of cardiac myocytes in rats, and the alteration is different at different regions. It is suggested that the difference or change of I Ca density (measured at an instant potential of 20% AP repolarization) is the cause of regional heterogeneity of APD of normal cardiac myocytes, and shortening of APD 20 of cardiac myocytes from FW in suspended rats.