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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。
To investigate the electrophysiological mechanism of cardioprotection of warm cardioplegia with lidocaine. Methods Whole-cell voltage-clamp technique and computer program (PCLAMPS, 51, AxonInstr.) Were used to record and analyze membrane potential and current. Results Lidocaine warm blood cardioplegia significantly inhibited the L-type calcium channel, and the action potential plateau disappeared, the duration shortened by 79.03% ± 3.1%; cold crystalloid cardioplegia for L- Calcium channel has no effect, action potential plateau is clearly visible, shorten the duration of 60.21% ± 46%. Conclusions Lidocaine warm blood cardioplegia has a slow calcium channel blocker property that protects cardiomyocytes from damage by avoiding intracellular calcium overload.