摘要
目的:探讨氨茶碱对体外循环(CPB)所致脑损伤的保护作用。方法:选择6~36月龄先天性房、室间隔缺损患儿40例,采用随机分组表分为氨茶碱组和对照组,每组20例。氨茶碱组于麻醉诱导后缓慢(5min)静脉注射氨茶碱(5mg/kg),其后按0.5mg/(kg·h)经微量泵持续静脉注射;对照组用等容量平衡盐溶液静脉注射。分别于CPB转机时(T1)、CPB停机时(T2)、停机后6h(T3)、24h(T4)采中心静脉血,用ELISA方法测定血清中S-100β蛋白和特异性烯醇化酶(NSE)水平以及血浆中肿瘤坏死因子-α(TNF-α)、白介素-8(IL-8)、白介素-10(IL-10)的浓度。结果:两组S-100β蛋白,NSE,TNF-α,IL-8水平均在转机后上升,CPB停机时(T2)达到高峰,停机后回落;两组IL-10在CPB后均增加。在T2和T3时点S-100β蛋白,NSE,TNF-α,IL-8水平氨茶碱组明显低于对照组(P<0.05或P<0.01),而IL-10明显高于对照组(P<0.05)。结论:婴幼儿CPB期间血清S-100β蛋白和NSE水平升高,即CPB过程中存在脑损伤。氨茶碱降低CPB过程中S-100β蛋白和NSE水平,可能是通过抑制炎症反应、调节促炎因子/抗炎因子之间的平衡。因此氨茶碱可能具有一定脑保护作用。
Objective To investigate the protective effect of aminophylline on cerebral injury induced by cardiopulmonary bypass ( CPB ) in infants. Methods Forty patients who underwent ventricular septal defect within 3 years old were randomly divided into 2 groups (20 cases in each group ). Aminophylline group : aminophylline (5 mg/kg ) was injected slowly via the vein after anesthesia and maintained at a dose of 0. 5 mg/ ( kg · h ) until the end of CPB. Control group : aminophylline was replaced by Ringer' s lactated solution. Samples were obtained at the beginning of CPB (T1) ,the end of CPB (T2) ,6 h (T3) and 24 h (T4) after the operation to measure S-100 β protein, NSE, tumor necrosis factor-α (TNF-α) , interleukin-8 (IL-8) , and interleukin-10 (IL-10 ) concentration by ELISA in the 2 groups. Results Compared with the time point immediately before CPB, the S-10013 protein,NSE, TNF-α, and IL-8 concentration in the 2 groups began to increase with the start of CPB, reached a climax at the end of CPB ( T2 ) , decreased gradually 6 h after the termination of CPB ( T3 ) and could not restore to the level before CPB at T4 ( 24 h after the termination of CPB). IL-10 in the 2 groups both increased after the CPB. At T2 and T3, S-100βprotein, NSE, TNF-α, and IL-8 concentrations were significantly lower than those in the aminophylline group (P 〈 0.05 or P 〈 0.01 ) , while IL-10 was just the opposite. Conclusion There is cerebral damage induced by CPB. Aminophylline may play a protective role in cerebral injury by modulating the balance between the pro-inflammatory factor and anti-inflammatory factor to reduce the level of S-100β protein and NSE during CPB and open cardiac surgeries.
出处
《中南大学学报(医学版)》
CAS
CSCD
北大核心
2009年第11期1126-1131,共6页
Journal of Central South University :Medical Science
基金
湖南省科委资助基金(06sk3014)~~