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目的 研究氙气干预对急性一氧化碳(CO)中毒迟发性脑病(DNS)大鼠模型的防治作用,临床治疗探索有效的治疗手段.方法 选择成年Wistar大鼠,随机分为持续干预组、早期干预组和对照组,腹腔注入CO(150 ml/kg)建立CO中毒DNS模型.持续干预组中毒后30 min腹腔注射氙气(150ml/kg),此后每日重复1次,持续2周,早期干预组最初3 d处理与持续干预组相同,中毒第4天改为每日腹腔注射等体积空气.对照组每日注射等体积空气.中毒后1～6周后水迷宫试验评估动物的智力状态,中毒后6周应用细胞外微电极记录海马齿状回长时程增强(long-term potentiat ion,LTP),此后取脑组织,皿染色观察病理改变,TUNEL法检测脑组织细胞凋亡.采用X2检验比较各实验组间DNS发病率,方差分析比较各实验组间HbCO含量和细胞凋亡率,组间比较采用两样本均数t检验,P＜0.05为差异具有统计学意义,统计分析软件SPSS 11.0辅助运算.结果 腹腔注入CO后,对照组大鼠出现智力下降,脑组织细胞凋亡明显.持续干预组和早期干预组大鼠智力改善,脑组织病理损害减轻,细胞凋亡率降低.海马齿状回LTP 发生率增加和幅度均显著高于对照组.持续干预组与早期干预组之间差异无统计学意义.结论 干预可有效降低CO中毒DNS发病率,显著减轻CO中毒DNS损害程度.早期干预与持续干预疗效相似.

Objective To investigate the effect of xenon intervention on delayed neuropsychologic sequelae (DNS)in acute carbon monoxide(CO)poisoning.Method Adult Wistar rats were randomly divided into sustained group,early intervention group,and control group.CO(150 ml/kg)was infused by intraperitoneal injection to produce DNS model.In sustained intervention group(S-group),xenon(150 ml/kg/d)was infilsed by intraperitoneal injection for 2 weeks;in control group(C-group),xenon was replaced by equal volume air;and in early intervention group(E-tvoup),xenon(150 ml/kg/d)was,employed in the first 3 days and air(150 ml/kg/d)was substituted for xenon in the following days until 2 weeks after CO poisoning.Morris maze test was used to evaluate the intelligence of rats.The long-term potentiation(LTP)of hippocampus Was detected by neuroelectricity recording.The apoptosis rates in brain was detected by TUNEL staining.The data were expressed as(x±s)and analyzed with student's test and analysis of variance.A P value less than 0.05 indicated statisfical significance.Results After exposure to CO,poisoned rats showed intelligence decline,demyeliation ofwater matler and cell apoptosis increased,which were consistent with DNS.In S-group and E-group,the rates of DNS and apoptosis were significantly lower than those in C-group,whereas the rote of LTP in S-group and E-group Was significantly higher than those in C-group.Conclusions Early xenon intervention can effectively decrease the rates of DNS occurred after acute CO poisoning.