摘要目的慢性压力负荷导致的心肌肥厚所伴有的动作电位时程的延长可能与L型钙流失活延迟有关. 本文的目的是探索左室高血压所致的家猫肥厚心肌的单通道L型钙流的特征,以及在动作电位延长中的作用.方法应用膜片钳技术研究正常和压力负荷所致的肥厚家猫心肌单通道L型钙流的特征.左室高血压模型用部分结扎降主动脉的方法.结果从-40?mV去极化到0?mV时,正常心肌和肥厚心肌的单通道L型钙流的振幅分别为1.02±0 .03?pA和1.05±0.03?pA,斜率电道分别为26.2±1.0?pS和25.8±0.9?pS,两者相比均无差别.但脉冲终末部分的平均振幅,肥厚心肌明显大于正常心肌.通道开放时间直方图分析表明,正常心肌细胞的开放时间分布呈单指数曲线,而肥大心肌细胞为双指数曲线 .肥大心肌的平均开放时间明显长于正常心肌细胞.结论左室压力负荷所致的肥大细胞的动作电位时程延长与L型钙流的失活时间延迟有关.

abstractsObjective To explore the mechanism underlying the prolongation of action potential and delayed inactivation of the L-type Ca2+ (ICa,L) current in a feline model of left ventricular system hypertension and concomitant hypertrophy.Methods Single Ca2+ channel properties in myocytes isolated from normal and pressure overloaded cat left ventricles were studied, using patch-clamp techniques. Left ventricular pressure overload was induced by partial ligation of the ascending aorta for 4-6 weeks. Results The amplitude of single Ca2+ channel current evoked by depolarizing pulses from -40mV to 0mV was 1.02±0.03pA in normal cells and 1.05±0.03pA in hypertrophied cells, and there was no difference in single channel current-voltage relationships between the groups since slope conductance was 26.2±1.0pS in normal and hypertrophied cells, respectively. Peak amplitudes of the ensemble-averaged single Ca2+ channel currents were not different between the two groups of cells. However, the amplitude of this averaged current at the end of the clamp pulse was significantly larger in hypertrophied cells than in normal cells. Open-time histograms revealed that open-time distribution was fitted by a single exponential function in channels of normal cells and by a two exponential function in channels of hypertrophied cells. The number of long-lasting openings was increased in channels of hypertrophied cells, and therefore the calculated mean open time of the channel was significantly longer compared to normal controls.Conclusion Kinetic changes in the Ca2+ channel may underlie both hypertrophy-associated delayed inactivation of the Ca2+ current and, in part, the pressure overload-induced action potential lengthening in this cat model of ventricular left systolic hypertension and hypertrophy.