摘要
目的探讨异丙酚对大鼠窒息性心脏停搏复苏后海马c—JUN氨基末端激酶（JNK）活化的影响。方法雄性sD大鼠40只，6月龄，体重350～380g，采用随机数字表法，将其分为4组（n=10），假手术组（s组）仅动静脉置管和气管插管而不制备窒息性心脏停搏；窒息性心脏停搏复苏组（CA—CPR组）采用窒息法建立CA—CPR模型；异丙酚组（P组）于窒息前30min静脉注射异丙酚20mg／kg，继之以40mg·k-1·h-1的速率静脉输注至复苏开始；生理盐水组（Ns组）以等容量生理盐水替代异丙酚，余处理同P组。成功复苏后12h时，处死大鼠，取脑组织，测定湿，干重（W／D）比；采用免疫组化法和Westernblot法测定海马磷酸化JNK（p-JNK）的表达水平，并观察海马病理学结果。结果与s组比较，CA．CPR组、P组和Ns组脑W／D比升高，海马p-JNK表达水平上调（P〈0．05或0．01）；与CA—CPR组比较，P组脑W／D比降低，海马p-JNK表达水平下调（P〈0．05或0．01），Ns组上述指标差异无统计学意义（P〉0．05）。P组海马病理学损伤较CA—CPR组减轻。结论异丙酚可抑制大鼠窒息性心脏停搏复苏后脑组织JNK的活化，从而减轻脑损伤。
Objective To investigate the effect of propofol on the activation of c-Jun N-terminal kinase （JNK） in hippocampus following asphyxial cardiac arrest-resuscitation in rats. Methods Forty male Sprague-Daw- ley rats, aged 6 months, weighing 350-380 g, were randomly divided into 4 groups （ n = 10 each） ： sham operation group （group S）, asphyxial cardiac arrest-cardiopulmonary resuscitation group （group CA-CPR）, propofol group （group P） and normal saline group （group NS）. All the rats were tracheostomized and mechanically ventilated after anesthetization. Cardiac arrest was induced by clamping the tracheal tube at the end of exhalation until ECG activi- ty disappeared and MAP 〈 10 mm Hg. Resuscitation was started 3 min later. MAP 〉 60 mm Hg and HR 〉 250 bpm were considered to be signs of successful resuscitation. Propofol 2 mg/kg was injected intravenously at 30 min before asphyxia, followed by propofol infusion at a rate of 4 mg＂ kg- 1 . h- l until the start of resuscitation in group P, while the equal volume of normal saline was given in group NS. At 12 h after successful resuscitation, the ani- mals were sacrificed and brains were harvested for determination of wet/dry brain weight （W/D） ratio in brain tis- sues and expression of phosphor-JNK （p-JNK） in hippocampus （by immuno-histochemistry and Western blot）, and for examination of the pathological changes of hippocampus. Results Compared with group S, W/D ratio was sig- nificantly increased and the expression of p-JNK in hippocampus was up-regulated in CA-CPR, P and NS groups （ P 〈 0.05 or 0.01 ）. Compared with group CA-CPR, W/D ratio was significantly decreased and the expression of p-JNK in hippocampus was down-regulated in group P （ P 〈 0.05 or 0.01 ）, and no significant change was found in the indexes mentioned above in group NS （P 〉 0.05）. The pathological changes of hippocampus were significantly attenuated in group P compared with group CA-CPR. Conclusion Propofol can inhibit the activation of
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
2013年第6期739-741,共3页
Chinese Journal of Anesthesiology
基金
徐州市医学科研项目（XWJ2011080）
