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内源性大麻素物质(endocannabinoid anandamde,AEA)可对抗缺血/再灌注所致心脏损伤和心律失常,但其电生理机制尚未完全明了。本文旨在利用细胞内微电极记录方法观察AEA对家兔窦房结自律细胞动作电位的影响,并探讨其机制。采用新西兰大白兔制备离体窦房结标本并记录动作电位,通过累计给药法给予窦房结标本不同浓度(1、10、100、200和500nmol/L)的AEA处理,部分标本在AEA(200nmol/L)处理前,分别给予大麻素1型(CB1)受体阻断剂AM251、大麻素2型(CB2)受体阻断剂AM630、非特异性K+通道阻滞剂tetraethylammonium(TEA)和NO合酶抑制剂L-nitro-arginine methylester(L-NAME)预处理。结果显示:(1)AEA(100、200和500nmol/L)可缩短家兔窦房结自律细胞的动作电位时程,降低动作电位幅度(P<0.05);(2)AM251可消除AEA缩短动作电位时程的作用,而AM630对此无影响;(3)TEA和L-NAME对AEA的作用无影响。结果提示,AEA可通过CB1受体降低家兔窦房结自律细胞动作电位幅度、缩短动作电位时程,此作用可能通过阻断Ca2+通道所实现,与K+通道及NO无关。
Endocannabinoid anandamde (AEA) can counteract the cardiac injury and arrhythmia caused by ischemia / reperfusion, but its electrophysiological mechanism is not fully understood. This article aims to use intracellular microelectrode recording method to observe the effect of AEA on the action potential of sino-atrial cells in rabbits and to explore its mechanism. New Zealand white rabbits were used to prepare ex vivo sinoatrial node specimens and the action potentials were recorded. AEA (1, 10, 100, 200 and 500 nmol / L) of different concentration (1, 10, 100, 200 and 500 nmol / (CB1) receptor blockers AM251, cannabinoid type 2 (CB2) receptor blockers AM630, non-specific K + channel blockers tetraethylammonium (TEA) and NO The synthase inhibitor L-nitro-arginine methylester (L-NAME) pretreatment. The results showed that: (1) AEA (100, 200 and 500 nmol / L) could shorten the action potential duration and decrease the amplitude of action potential (P <0.05); (2) AM251 can eliminate AEA shortening action Potential duration, AM630 had no effect on this; (3) TEA and L-NAME had no effect on AEA. The results suggest that AEA can reduce the amplitude of action potential and decrease the action potential duration of sarcoplasmic sarcolemma via CB1 receptor. This effect may be achieved by blocking Ca2 + channel, and has nothing to do with K + channel and NO.