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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 缩短的原因
Objective To observe the change of action potential (AP) of cardiomyocytes in 4-week simulated weightlessness and further elucidate its ion mechanism. Methods The rat model of tail suspension was used to simulate weightlessness. Cardiomyocytes were isolated by collagenase and the membrane capacitance, AP, transmembrane inward calcium current (ICa) and transient outward potassium current (Ito) of single cardiomyocytes were recorded by patch clamp. Wait. Results The APD of left ventricular free wall in normal control rats was longer than that of apex (P <0.05). APD20 of left ventricular free wall myocytes in suspension group was shorter than that in control group (P <0.01), but not in the apex. In the control group, the ICa density of left ventricular free wall cells (AP) was greater than that of the apex (P <0.05). In the left ventricular free wall, the density of ICa in the suspension group was smaller than that in the control group (P <0.05). Conclusions The APD of myocardial cells in different parts of left ventricle in normal rats is non-uniform. Simulated weightlessness 4 weeks can induce changes of APD20 in rat cardiomyocytes with different sites. The ICa of 20% real-time potentials in repolarization varied or changed Is caused by non-homogeneity of APD sites in normal cardiomyocytes and shortening APD20 of isolated left ventricular myocardium after simulated weightlessness