“缺血”引起的绵羊浦肯野纤维跨膜电位与离子流变化

THE CHANGES OF TRANSMEMBRANE POTENTIAL AND IONIC CURRENTS INDUCED BY "ISCHEMIA"IN SHEEP CARDIAC PURKINJE FIBERS

以低氧、高钾、低pH、无能量供应的模拟缺血溶液灌流离体绵羊心脏浦肯野纤维,观察“缺血”对心肌跨膜电位和离子流的影响。实验共24例。跨膜电位的变化过程如下:模拟缺血液灌流后2-3min,首先出现最大舒张电位(MDP)轻度除极,4期舒张除极速率减慢,随后动作电位时程(APD)缩短(n=13)或先缩短、后延长、再缩短的变化(n=11),平台逐渐消失,最后MDP进一步除极,动作电位波幅(APA)减小,兴奋性逐渐降低,以致不能引出动作电位(AP)。其中6例即使MDP高于-60mV时AP已不能引出。以上变化过程历时长短不等,在不同标本为30-160min。跨膜离子流方面,当APD缩短时,在所有膜电位水平即时外向电流都明显增加。稳态电流-电压关系曲线由正常的S形变成直线,内向整流现象消失。慢内向离子流由“缺血”前的6.74±4.48nA减少到0.86±1.39nA,(M±SD,P<0.01,n=8),在多数测试电位水平都有显著减少,其电流-电压关系曲线向较负电位方向移位。以上结果提示:心肌“缺血”时浦肯野细胞起搏功能受抑制,细胞内大量K^+外流,Ca^(2+)内流减少,心肌细胞除极,以上多种变化可能为心肌缺血时心律失常发生的原因。

Ischemia-mimic solution (hypoxia, hyperkalemia, acidosis, no substrate) in-duced changes of transmembrane potential and ionic current were observed in24 sheep cardiac Purkinje fibers. The sequence of changes of transmembranepotential was as follows: Two to three min after perfusion with ischemiamimicsolution, the maximum diastolie potential (MDP) was depolarized slightly, andattended by a decrease of depolarization rate of phase 4 while the action potentialduration (APD) was shortened or underwent a shortening-prolongation-reshor-tening process. Then, the plateau of action potential disappeared gradually. AsMDP was depolarized further, the action potential amplitude (APA) and the excit-ability of the Purkinje fibers decreased continuously until action potential could nolonger be elicited. The whole process took 30min to 160min in different preparations. When the APD was shortened, the instantaneous outward current was alwaysincreased at all membrane potential levels. The steady-state current-voltagerelationship (CVR) curve was changed from S shape to a straight line, and theinward rectification phenomenon disappeared. Under ischemic condition, theamplitude of I_(si) was decreased from 6.74±4.48 nA to 0.86±1.39 nA, and theCVR curve shifted more to the negative. The above results indicate that under the ischemic condition, the pacemakerfunction of cardiac Purkinje cell is inhibited, a large amount of K^+ ions outflowsand inward current I_(si) is decreased. These changes may be the reasons for thegenesis of ischemic arrhythmia.