Objective:To study the effect of propofol and isoflurane general anesthesia on nerve injury in patients with craniocerebral trauma after emergency surgery.Methods:Patients with craniocerebral trauma who accepted emergency surgery in Dangyang People's Hospital between May 2015 and February 2017 were selected and randomly divided into propofol group and isoflurane group who received propofol + fentanyl + vecuronium bromide as well as isoflurane + fentanyl + vecuronium bromide anesthesia respectively.Serum levels of nerve injury markers,excitatory amino acids,inhibitory amino acids and oxi-dative stress indicators were detected before operation,immediately after operation and 12 hours after operation.Results:Im-mediately after operation and 12 hours after operation,serum NSE,GFAP,NGB,Tau,GLU,ASP,8-iso-PGF2α and MDA levels of both groups of patients were significantly lower than those before operation while GABA,ALA,HO-1,NQO-1 and SOD levels were significantly higher than those before operation(P< 0.05),and serum NSE,GFAP,NGB,Tau,GLU, ASP,8-iso-PGF2α and MDA levels of propofol group immediately after operation and 12 hours after operation were significant-ly lower than those of isoflurane group while GABA,ALA,HO-1,NQO-1 and SOD levels were significantly higher than those of isoflurane group(P< 0.05).Conclusion:Propofol for emergency surgery of patients with craniocerebral trauma is more effective than isoflurane in alleviating nerve injury degree,correcting the excitatory and inhibitory amino acid disorder, and inhibiting oxidative stress reaction.%目的:研究丙泊酚与异氟烷全身麻醉对颅脑外伤患者急诊手术后神经损伤程度的影响.方法:选择2015年5月~2017年2月期间在当阳市人民医院接受急诊手术治疗的颅脑外伤患者,随机分为丙泊酚组和异氟烷组,分别接受丙泊酚+芬太尼+维库溴铵以及异氟烷+芬太尼+维库溴铵麻醉.手术前、手术后即刻、手术后12小时,检测血清中神经损伤标志物、兴奋性氨基酸和抑制性氨基酸、氧化应激指标的含量.结果:手术后即刻、手术后12小时,两组患者血清中 NSE、GFAP、NGB、Tau、GLU、ASP、8-iso-PGF2α、MDA的含量均显著低于手术前,GABA、ALA、HO-1、NQO-1、SOD的含量均显著高于手术前(P<0.05)且丙泊酚组患者手术后即刻、手术后12小时血清中 NSE、GFAP、NGB、Tau、GLU、ASP、8-iso-PGF2α、MDA的含量均显著低于异氟烷组,GABA、ALA、HO-1、NQO-1、SOD 的含量均显著高于氟烷组(P<0.05).结论:丙泊酚用于颅脑外伤患者急诊手术能够较异氟烷更为有效的减轻神经损伤程度、纠正兴奋性氨基酸和抑制性氨基酸紊乱、抑制氧化应激反应.
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