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作 者:宋晓阳[1] 王焱林[2] 甘国胜[1] 陈利民[1] 王成夭[2] 丘伟[3]
机构地区:[1]广州军区武汉总医院麻醉科,武汉430070 [2]武汉大学中南医院麻醉学教研室,武汉430071 [3]广州军区武汉总医院中心实验室,武汉430070
出 处:《中国康复》2007年第2期99-101,共3页Chinese Journal of Rehabilitation
摘 要:目的:观察丙泊酚对颅脑外伤患者手术期间血清神经元特异性烯醇化酶(NSE)的影响及与术后6个月时简易智能量表(MMSE)评分的相关性。方法:30例颅脑外伤患者随机分为2组各15例,均于手术时分别采用丙泊酚(A组)和异氟醚(B组)麻醉。于手术前及手术开始2h、手术结束时测定血清NSE含量;6个月后以MMSE量表对2组接受随访的患者进行评分。结果:手术2h和手术结束时与手术前比较,2组NSE均升高,手术结束时2组间比较A组NSE低于B组(P<0.05);2组手术结束时NSE含量与6个月后MMSE评分呈显著负相关(r=-0.469,P<0.05),A组MMSE评分高于B组,但差异无显著性意义。结论:血清NSE含量的高低可作为判断患者预后的重要指标,临床麻醉剂量的丙泊酚可以降低手术期间NSE的升高,改善预后,具有脑保护作用。Objective: To investigate the effect of propofol on serum concentration of neuron specific enolase (NSE) in patients undergoing neurosurgery and its relation with the MMSE score 6 months after operation. Methods: Thirty patients with cerebral injury were randomly divided into 2 groups: propofol group (n= 15) and isoflurane group (n= 15). The serum concentration of NSE was measured before operation,2 h after operation beginning and after operation. Twenty-three out of 30 patients with cerebral injury were followed up 6 month later,and the MMSE scores were also estimated and recorded. Results: The serum concentration of NSE 2 h after operation beginning and after operation was higher than that before operation. The concentration in propofol group was significantly lower than that in isoflurane group after operation (P〈0.05); The concentration after operation was significantly negatively correlated with the MMSE scores of the patients 6 month later (r=-0. 469, P〈0.05). MMSE scores in propofol group were higher than in isoflurane group, but there was no significant difference between them. Conclusion: The serum concentration of NSE is increased in the patients with cerebral injury. The NSE concentration at the end of operation was a useful marker for the occurrence of postoperative neuropsycholatic dysfunction. The anesthesia dose of propofol by intravenous pumping can reduce the increase of the serum concentration of NSE,improve the postoperative dysfunction,and exert a protective influence on the brain.
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