颈内动脉输注异丙酚对胶质瘤切除术患者的脑保护作用

目的 探讨颈内动脉输注异丙酚对胶质瘤切除术患者的脑保护作用.方法 择期胶质瘤切除术患者40例和立体定向胶质瘤活检术患者20例,年龄40～64岁,体重48～73 kg.采用随机数字表法,将拟行胶质瘤切除术患者随机分为2组(n=20):颈内动脉给药组(IA组)和静脉给药组(Ⅳ组).拟行立体定向胶质瘤活检术患者为对照组(C组),采用2%利多卡因15～20 ml术野局部浸润麻醉.IA组和Ⅳ组采用异丙酚-瑞芬太尼-罗库溴铵行麻醉诱导.IA组麻醉诱导后行颈内动脉穿刺置管,颈内动脉靶控输注异丙酚.两组术中调整异丙酚和瑞芬太尼靶浓度,维持BIS值40～60.间断静脉注射罗库溴铵.术中取胶质瘤组织标本,采用免疫组化法测定胶质瘤组织水通道蛋白1(AQP1)和AQP4表达.于麻醉诱导前(T1)、切皮时(T2)、术毕时(T3)、拔除气管导管时(T4)记录MAP和HR;记录手术时间、麻醉用药情况.结果 与T1时比较,Ⅳ组T2,3时MAP和HR降低(P＜0.05),IA组各时点MAP和HR比较差异无统计学意义(P＞0.05).与IA组比较,Ⅳ组MAP和HR降低(P＜0.05).与C组比较,IA组和Ⅳ组AQP1和AQP4表达下调(P＜0.05).与Ⅳ组比较,IA组异丙酚用量减少(P＜0.05),AQP1和AQP4表达、瑞芬太尼和罗库溴铵用量、手术时间比较差异无统计学意义(P＞0.05).结论 与静脉输注异丙酚相比,颈内动脉途径给药不仅可减少胶质瘤切除术患者异丙酚的用量,而且对其脑保护作用没有影响.

Abstract：

Objective To investigate the cerebral protective effect of intracarotid infusion of propofol in patients undergoing resection of cerebral gliomas. Methods Sixty ASA Ⅰ- Ⅲ patients with cerebral glioma aged 40-64 yr weighing 48-73 kg were enrolled in this study. Forty patients undergoing resection of glioma under general anesthesia were randomly divided into 2 groups ( n = 20 each): intracarotid propofol group (group IA ) and intravenous propofol group (group Ⅳ). Twenty patients undergoing biopsy of glioma under local infiltration anesthesia with 2% lidocaine 15-20 md served as control group (group C). In IA and Ⅳ groups anesthesia was induced with TCI of propofol and remifentanil. Tracheal intubation was facilitated with rocuronium 0.6 mg/kg. The patients were mechanically ventilated. PErCO2 was maintained at 35-45 mm Hg. Anesthesia was maintained with TCI of propofol and remifentanil and intermittent iv boluses of rocuronium. In group IA internal carotid artery was cannulated after induction of anesthesia and propofol was administered by TCI via carotid artery while remifentanil was administered by TCI via peripheral vein. BIS was maintained at 40-60 during operation. ECG, MAP, HR, SpO2, PETCO2 and BIS were continuously monitored. MAP and HR were recorded before induction of anesthesia (T1) ,during skin incision (T2 ), at the end of operation (T3), during extubation ( T4 ). The glioma specimens were obtained for microscopic examination and determination of aquaporin 1 and aquaporin 4 ( AQP1, AQP4) expression by immunohistochemistry. Results MAP and HR were significantly decreased at T2 and T3 as compared with the baseline at T1 in group Ⅳ ( P ＜ 0.05), while there was no significant change in MAP and HR after induction of anesthesia in group IA ( P ＞ 0.05). The expression of AQP1 and AQP4 was down-regulated in IA and Ⅳ groups compared with group C (P ＜0.05). The propofol consumption during anesthesia was significantly less in group IA than in group Ⅳ (P ＜0.05). There was no significant diffe-rence in AQP1 and AQP4 expression, the amount of remifentanil and recuronium consumed and duration of operation betweenIA and Ⅳ groups ( P ＞ 0.05). Concltsion Intracarotid propofol can decrease the amount of propofol needed for maintenance of anesthesia as compared with intravenous administration and attenuate brain edema,indicating cerebral protective effect.

Cerebral protective effect of intracarotid propofol in patients undergoing resection of cerebral gliomas

Objective To investigate the cerebral protective effect of intracarotid infusion of propofol in patients undergoing resection of cerebral gliomas. Methods Sixty ASA Ⅰ- Ⅲ patients with cerebral glioma aged 40-64 yr weighing 48-73 kg were enrolled in this study. Forty patients undergoing resection of glioma under general anesthesia were randomly divided into 2 groups ( n = 20 each): intracarotid propofol group (group IA ) and intravenous propofol group (group Ⅳ). Twenty patients undergoing biopsy of glioma under local infiltration anesthesia with 2% lidocaine 15-20 md served as control group (group C). In IA and Ⅳ groups anesthesia was induced with TCI of propofol and remifentanil. Tracheal intubation was facilitated with rocuronium 0.6 mg/kg. The patients were mechanically ventilated. PErCO2 was maintained at 35-45 mm Hg. Anesthesia was maintained with TCI of propofol and remifentanil and intermittent iv boluses of rocuronium. In group IA internal carotid artery was cannulated after induction of anesthesia and propofol was administered by TCI via carotid artery while remifentanil was administered by TCI via peripheral vein. BIS was maintained at 40-60 during operation. ECG, MAP, HR, SpO2, PETCO2 and BIS were continuously monitored. MAP and HR were recorded before induction of anesthesia (T1) ,during skin incision (T2 ), at the end of operation (T3), during extubation ( T4 ). The glioma specimens were obtained for microscopic examination and determination of aquaporin 1 and aquaporin 4 ( AQP1, AQP4) expression by immunohistochemistry. Results MAP and HR were significantly decreased at T2 and T3 as compared with the baseline at T1 in group Ⅳ ( P ＜ 0.05), while there was no significant change in MAP and HR after induction of anesthesia in group IA ( P ＞ 0.05). The expression of AQP1 and AQP4 was down-regulated in IA and Ⅳ groups compared with group C (P ＜0.05). The propofol consumption during anesthesia was significantly less in group IA than in group Ⅳ (P ＜0.05). There was no significant diffe-rence in AQP1 and AQP4 expression, the amount of remifentanil and recuronium consumed and duration of operation betweenIA and Ⅳ groups ( P ＞ 0.05). Concltsion Intracarotid propofol can decrease the amount of propofol needed for maintenance of anesthesia as compared with intravenous administration and attenuate brain edema,indicating cerebral protective effect.