丙泊酚对颅内动脉瘤夹闭术患者术后认知障碍的机制研究

The mechanism of postoperation cognitive dysfunction in postoperative patients receiving intracranial aneurymn clipping

目的探讨丙泊酚对颅内动脉瘤夹闭术患者术后脑脊液氧化应激标记物和tau蛋白的影响,探讨术后认知障碍发生机制。方法择期拟行颅内动脉瘤夹闭术患者40例,随机分为两组:丙泊酚组(P组)和七氟烷组(S组),每组20例。两组全麻诱导气管插管后行机械通气,麻醉维持:P组靶控输注(TCI)丙泊酚,血浆浓度为2~4μg/mL,S组吸入七氟烷(MAC 1.0~2.0),两组同时TCI瑞芬太尼,血浆浓度为2~4 ng/mL,阿曲库铵(肌松监测下使用)维持麻醉平稳。分别于麻醉前(T0)、术后6 h(T1)、24 h(T2)、48 h(T_3)、72 h(T4)时收集脑脊液2 mL,测定脑脊液8-异前列腺素F2α(8-isoPGF2α)、超氧化物歧化酶(SOD)、总tau(T-tau)蛋白、磷酸化tau蛋白(P-tau)的浓度。结果与T0时比较,两组T_1,T_2,T_3,T4时的PGF2α、T-tau、P-tau蛋白浓度均有明显升高,SOD活性P组无明显变化,而S组明显降低;与S组比较,P组T_1,T_2,T_3,T4时8-iso-PGF2α、T-tau和P-tau蛋白水平均降低,SOD活性升高。结论丙泊酚可通过抗氧化作用降低颅内动脉瘤夹闭术患者脑脊液内8-iso-PGF2α及tau蛋白磷酸化水平。

Objective To investigate the effect of propofol on the markers of oxygen stress and tau protein in cerebral fluid in postoperative patients of intracranial aneurysms after clipping and The mechanism of postoperation cognitive dysfunction.Methods Forty patients undergoing elective intracranial aneurysm clipping were randomized into2groups(n=20each):propofol(group P)and sevoflurane group(group S).Anesthesia was induced with propofol,fentanyl and atracurium and maintained with sevoflurane(MAC1.0～2.0)in group S and TCI of propofol(Cp2～4μg/mL)in group P respectively.At the same time,combination of TCI of remifentanil(Cp2～4ng/mL)and continuous rate infusion of atracurium(7-10ml/h).CSF concentrafions of8-iso-PGF2α(by ELISA),SOD(by Xanthine-oxidation method),T-tau and P-tau protein(by double-Sandwich ELISA)were measured respectively before operation(T0),6hours(T1),24hours(T2),48hours(T3)and72hours(T4)after operation.Results At T1,T2,T3and T4the CSF concentrations of8-iso-PGF2α,tau protein and P-tau protein were significantly lower in group P than in group S,while the activity of SOD is significantly higher in group P than in group S.Conclusion Propofol can decrease the oxygen stress and tau protein in cerebral fluid through antioxidative effects on brain after operation in patients undergoing clipping of intro-cranial aneurysm.