异丙酚麻醉中大脑皮质体感诱发电位变化的作用机制

Study on the mechanisms on somatosensory evoked potentials during propofol anesthesia

目的:探讨中枢性去甲基肾上腺素(NA)机制在异丙酚麻醉中大脑皮质体感诱发电位(SEP)变化中的作用。方法:SD雄性大鼠15只,体重220～250 g,右侧海马内植入微透析探头,按国际脑电10/20系统法安置银针头皮电极,左侧前爪腕部正中神经处安置刺激电极,强度5.2 mA,刺激间隔0.2 ms。动物随机分为3组。A组:经微量泵依次以10、60 mg·kg^(-1)·h^(-1)静滴异丙酚各45 min后停止给药直至动物清醒。B组和C组于开始输注异丙酚的同时分别腹腔内注射α2-肾上腺素受体激动剂(可乐定)或拮抗剂(育亨宾)0.5 mg/kg,其余操作和A组相同。分别于麻醉前(基础值)、麻醉中不同浓度给药时及苏醒期经微透析管收集透析液,检测海马细胞外液中NA浓度,记录皮质SEP N_(20)波的潜伏期和波幅。结果:①各指标基础值各组间差异无显著性(P>0.05)。②A组和B组海马NA释放在异丙酚以60 mg·kg(-1)·h^(-1)给药时与基础值相比均降低(P<0.05),B组更为明显,C组则随着异丙酚给药浓度增加直至停药后麻醉恢复期均显著增高(P<0.05)。③3组动物SEP N_(20)波潜伏期均无明显变化(P>0.05)。④A组不影响SEP N_(20)波幅(P>0.05);B组在异丙酚低浓度、高浓度给药期和麻醉恢复期SEP N_(20)波幅与基础值相比均显著减低,而C组则增高(P<0.05)。结论:α2-肾上腺素受体激动剂和抑制剂所引起的海马NA释放与SEP N_(20)波幅变化的一致性可能与镇痛有关,而异丙酚对海马NA释放的抑制可能是一种催眠反应。

Objective： To clarify the effect of mechanism of central noradrenaline （NA） on the changes in soma- tosensory evoked potentials （SEP） during propofol anesthesia. Methods：The microdialysis probe was implanted into the right hippocampus of the rats. According to the international electroencephalogram 10/20 system, silver needle electrodes were inserted in the scalp of rat receiving input, with impulse strength of 5.2 mA and interval time of 0. 2 ms, from the stimulatory electrode which was set in the median nerve on the left wrist of the forelimbs. Fifteen adult male SD rats, with an average body weight of 220 - 250 g, were randomly divided into 3 groups. In group A, the rats were infused intravenously with propofol at a rate of 10 mg·kg-1·h-1 for 45 minutes and then 60 mg·kg-1·h-1 for 45 minutes, and the rats were allowed to wake up. After the intraperitoneal injection of clonidine 0. 5 mg/kg in group B or yohimbine 0.5 mg/kg in group C, the rats were infused intravenously with propofol at the same rate as group A, and the rats were allowed to wake up. The NA in the extra-cel- lular liquid of hippocampus and the latency and amplitude of SEP N20 waves were quantified simultaneously before, during and emergence from anesthesia. Results： The baselines of the 3 parameters were not different among the 3 groups. Compared with the baselines, the NA release in hippocampus decreased in the period of propofol 60 mg·kg-1·h-1 in group A and B, and the decrease was more evident in group B （P〈0.05）. However, the NA release in C group increased significantly during the period of the propofol 10 mg·kg-1·h-1 , 60 mg·kg-1·h-1 and cessation of use of propofol （P^0. 05）. The latency of SEP N20 waves showed no change in the three groups（P〉0. 05）. Compared with the baseline,The amplitude of SEP Nz0 waves was not changed in group A, but redueed in group B and became higher in group C during the period of the propofol 10 mg·kg-1·h-1 , 60mg·kg-1·h-1 and the period of cessation of propofol （P〈0. 05）. Conclusions：The coherence in changes in ae-NA release in hippocampus and the amplitudes of SEP N20 waves were induced by the α2-NA receptor agonists, and antagonist is probably related with analgesic mechanism of α2-NA receptor, but the inhibition of NA release in hippoeampus caused by propofol may indicate one of hypnosis response from propofol.