乌司他丁对心肺复苏后大鼠血清神经元特异性烯醇化酶的影响及作用

目的：探讨心肺复苏后大鼠血清神经元特异性烯醇化酶（NSE）的变化、大脑皮层病理改变及乌司他丁的干预作用。方法：成年雄性SD大鼠120只,随机分为假手术对照组、复苏组、乌司他丁组（药物组）,每组按气管切开后（对照组）或自主循环恢复（ROSC）后（复苏组、药物组）0.5、3、6、12h和24h分为5个亚组（n=8）。复苏组和药物组采用窒息致大鼠心脏骤停和心肺复苏模型,药物组于ROSC后2min内经颈动脉推注乌司他丁（100000U/kg）。对照组仅行麻醉、气管切开和血管穿刺。各组分别于各时间点取血和组织标本,以ELISA法检测血清NSE浓度,光镜下观察大脑皮层的病理改变。结果：与对照组比较,复苏组和药物组ROSC后各亚组各时间点血清NSE含量明显升高（P〈0.05或P〈0.01）;与复苏组比较,药物组ROSC后6、12、24h血清NSE含量显著降低（P〈0.05或P〈0.01）。药物组病理损害轻于复苏组。结论：乌司他丁通过降低血清NSE浓度对心肺复苏后脑损伤具有一定的保护作用。

Influence of ulinastatin injection on serum neuron-specific enolase in rats after cardiopul-monary resuscitation

Objective： To investigate the serum concentration of neuron-specific enolase （NSE） and the histopathological changes of cerebral cortex in asphyxia rats with bolus ulinastatin for injection after cardiopulmonary resuscitation （CPR）. Methods ： One hundred and twenty male adult SD rats were randomly divided into 3 groups： sham-operation control group, CPR group and Ulinastatin group. Each group was divided into 5 subgroups （n=8） by various intervals （at 0.5, 3, 6, 12, 24 h after tracheotomy in control group or after ROSC in CPR group and ulinastatin group）. Asphyxiation cardiac arrest and CPR model was used in （PR group and Ulinastatin group,with bolus ulinastatin for Injection 100 000 U/kg via arteria carotis within 2 min after ROSC. Anaesthesia, tracheotomy and vascular centesis were performed in rats without asphyxiation in sham-operation group. Samples were taken at each intervals of subgroups. Serum levels of NSE were measured with enzyme-linked immunosorbent assay （ELISA）. The pathological changes of cortex were observed under light microscope. Results ： The serum levels of NSE elevated significantly after ROSC in CPR group and ulinastatin group than those in control group （P〈0.05 or P〈0.01）. Serum NSE level decreased at 6, 12 and 24 h after ROSC in ulinastatin group compared with CPR group （P〈O.05 or P〈0.01）. There were milder pathological changes in ulinastatin group than those in CPR group. Conclusion： Ulinastatin can alleviate cerebral injury after cardiopulmonary resuscitation by decreasing the level of serum neuron-speclfic enolase.