用心室压力钳方法研究家兔左心室单相动作电位的变化

目的构建小动物心室压力钳方法,观察机械刺激对心脏电活动的影响,探索心脏机械电反馈现象及其机制。方法应用自行构建的心室压力钳方法,在心室肌细胞动作电位末期牵张左心室,观察心室单相动作电位时程的变化。结果当左心室分别被强度为130 mmHg、140 mmHg、150 mmHg的额外牵张刺激钳制时,左室MAPD90〔单相动作电位复极90%的时程(monophasicaction potential duration upstroke to the level of 90%)〕较正常分别延长15.4%、26.1%、44.4%(P<0.05),左室MAPD20、MAPD50无明显变化;牵张前后右室MAPD20、MAPD50及MAPD90均无明显变化。结论自行构建的心室压力钳方法能较准确地模拟生理、病理生理条件下心室内的负荷变化情况,并能灵活地对心脏施加机械刺激,为在器官水平上研究心脏机械电反馈(mechano-electricfeedback,MEF)提供了压力控制方法上的改进;左心室复极末期牵张刺激可引起其心肌细胞动作电位时程(action potential duration,APD)延长、复极减慢,右室则无明显改变,提示该刺激直接导致了左心室上内向电流的发生。

Changes of Monophasic Action Potential in Rabbit Left Ventricles Induced by Ventricular Pressure-Clamping Method

Objective To establish a ventricular pressure-clamping method for isolated perfused hearts of small animals, observe the effect of mechanical stimuli on cardiac electrical activities and explore the phenomena and mechanisms of cardiac mechano-electric feedback. Methods Using the ventricular pressure-clamping method to stretch the left ventricle(LV) during the end of action potential, the effect on monophasic action potential duration(MAPD) of ventricles was observed. Results LVMAPD90 was lengthened by 15.4%, 26.1%, 44.4％(P<0.05) comparing to the control when the left ventricle was clamped by extra stretch which was 130, 140, 150 mmHg, respectively, while LVMAPD₂₀ and LVMAPD₅₀ had no changes; There was no significant difference in RVMAPD₂₀, RVMAPD₅₀ and RVMAPD₉₀ between before and after extra inflations were applied. Conclusion This ventricular pressure-clamping method developed by our lab can exactly mimic the changes of load in hearts under the physiological/pathophysiological conditions and can freely deliver mechanical stimuli to the ventricle, which improved the method of pressure-controlling on researching cardiac MEF at organ level; stretching the left ventricle during the end of the action potential could lengthen MAPD, slower repolarization, while the right ventricle had not the same changes, which suggested that the inflations caused a kind of inward current in the left ventricle.