【摘要】 目的 选用大鼠常温窒息性复苏模型,观察异丙酚、氯胺酮对脑缺血/再灌注的保护作用,并探讨其作用机制。方法 选取SD大鼠120只,在面罩下吸入异氟醚麻醉诱导,气管插管后机械通气,异氟醚吸入维持麻醉。随机分为4组:A组为假手术组,B组为对照组仪吸入异氟醚;C组为异氟醚复合异丙酚组;D组异氟醚复合氯胺酮组,每组30只。C组、D组分别在麻醉平稳后窒息前10min腹腔内注射异丙酚10 mg/100 g、氯胺酮10 mg/100 g。夹闭气管导管导致窒息性循环停止。10 min后行心肺复苏,在自主循环建立后30 min(T1)、120 min(T2)、180 min(T3),每组分别取7只大鼠,取动脉血及脑,测定脑组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量及动脉血血清肿瘤坏死因子α(TNF-α)和白介素1β(IL,1β)的浓度。结果 与B组相比,C组、D组SOD活性升高,MDA含量降低,TNF-α和IL-1β水平降低(P<0.05)。与A组比较,C组、D组SOD活性降低(P<0.01),C组仅在T1时点MDA含量升高(P<0.01),C组、D组在T2、T3时点血清TNF-α、IL-1β浓度升高(p<0.05)。结论异丙酚、氯胺酮对心肺复苏后大鼠脑组织具有一定的保护作用。更多还原

【Abstract】 Objective To investigate the cerebral protective effects of propofol and ketamine against ischemia-reperfusion injury induced by cardiac arrest in rats. Methods One hundred and twenty male SD rats weighing 180-250 g were randomly divided into four equal groups of 30 animals : group A served as control without cardiac arrest;group B was subjected to 10 minutes of cardiac arrest followed by resuscitation ( C-R); group C received propofol 10 mg 100 ·g-1 ip 10 min before C-R; group D received ketamine 10 mg-100· g-1 ip 10 min before C-R. The animals were anesthetized with isoflurane inhalation by mask, intubated and mechanically ventilated. Anesthesia was maintained with isoflurane inhalation. Cardiac arrest was induced by asphyxiation (vecuronium 0.01 mg - 100 g -1, disconnection of ventilator, tracheal tube clamping) and maintained for 10 min, then resuscitated. Seven animals in each group were killed at 30 min (T, ) , 120 min (T,) and 180 min (T3 ) after successful resuscitation respectively for determination of serum TNF-a and IL-Ip and cerebra) SOD activity and MDA content. Results Cerebral SOD activity in group C and D was significantly lower than that in group A but higher than that in group B, while cerebral MDA content in group C and D was significantly higher than that in group A but lower than that in group B ( P < 0.05 or 0.01) . Serum TNF-a and IL-Iμ levels were significantly increased in group C and D at T, and T, ( P < 0.01). Conclusion Propofol and ketamine can protect brain against ischemia-reperfusion injury through their anti-oxidant and anti-inflammatory effects.更多还原