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目的 探讨异丙酚的麻醉作用机理。方法 分别制备１０只成年ＳＤ大鼠大脑皮层突触体。实验分为ＫＣｌ组（突触体悬液中均加入２０ｍ ｍ ｏｌ·ｍ ｌ－ １ＫＣｌ）和氨基吡啶组（突触体悬液中加入６．７ｍ ｍ ｏｌ·ｍ ｌ－ １ 氨基吡啶）。每组又分为５ 个亚组，分别对应于突触体悬液中异丙酚浓度为０、１２．５、２５、５０ 和１００μｍ ｏｌ·ｍ ｌ－ １。谷氨酸的释放量由连续酶标荧光法测定。结果 异丙酚对ＫＣｌ组突触体谷氨酸释放量无显著抑制作用；而对氨基吡啶组突触体谷氨酸则有显著抑制作用，且呈剂量依赖性。结论 ＫＣｌ和氨基吡啶作用的差别仅在于ＫＣｌ不引起Ｎａ＋ 通道开放，而氨基吡啶则导致Ｎａ＋ 通道开放。异丙酚对两组突触体谷氨酸释放的不同影响表明，异丙酚主要通过阻断Ｎａ＋ 通道开放，减少中枢神经系统主要的兴奋性神经递质谷氨酸的释放而产生麻醉效能。
Objective To investigate the anesthetic mechanism of propofol. Methods The cortical synaptosomes of 10 adult SD rats were prepared respectively. The experiment was divided into KCl group (20mmol · ml-1KCl in the synaptosomal suspension) and aminopyridine group (6.7mol · ml-1 aminopyridine was added into the synaptosome suspension). Each group was subdivided into 5 subgroups, corresponding to concentrations of propofol of 0, 12.5, 25, 50 and 100 μmol · m l-1, respectively, in the synaptosomal suspension. The release of glutamic acid was determined by continuous enzymatic fluorimetry. Results Propofol had no significant inhibitory effect on glutamate release from synaptosomes in KCl group, while glutamate on aminopyridine group had a significant inhibitory effect on glutamate release in a dose-dependent manner. Conclusion The difference between KCl and aminopyridine only lies in that KCl does not cause Na + channel to open while aminopyridine leads to Na + channel to open. The different effects of propofol on the release of glutamate from both synapses suggest that propofol exerts its anesthetic effect by blocking the opening of Na + channels and decreasing the release of glutamate, the major central nervous system excitatory neurotransmitter.