摘要
探讨利多卡因温血心停搏液心肌保护的电生理机制。方法应用全细胞电压钳技术和计算机程序(PCLAMPS、51,AxonInstr.)记录和分析膜电位和电流。结果利多卡因温血心停搏液明显抑制了L-型钙通道,并使动作电位平台期消失,时程缩短了79.03%±3.1%;冷晶体心停搏液对L-型钙通道无作用,动作电位平台期明显可见,时程缩短了60.21%±46%。结论利多卡因温血心停搏液具有慢钙通道阻滞剂特性,它可通过避免细胞内钙超载而保护心肌细胞受损。
Objective To investigate the electrophysiologic mechanism of lidocaine warm blood cardioplegia (LWBCP) on its myocardial protection. Method Whole cell voltage-clamp technique and computerprogram were used to record and analyze the membrane potential and current. Result The LWBCP greatlyinhibited the amplitude of the peak Ca2+ inward current, the plateau was not seen and the action potential duration was shortened by 79. 03% ±3.1%. The cold crystalloid cardioplegia (CCP) had no effect on L-typeCa2+ inward current, the plateau was observed each time and the action potential duration was shortened by60.21%±4.6%. Conclusion The LWBCP was characterized by a slow calcium channel blocker. It wouldprotect myocardium from damage by avoiding the intracellular calcium overload.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
1999年第2期108-109,共2页
Chinese Journal of Experimental Surgery