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作 者:翟明玉[1] 顾尔伟[1] 张雷[1] 陈立建[1] 朱燕[1] 吴云[1] 刘训芹[1]
机构地区:[1]安徽医科大学第一附属医院麻醉科,合肥市230022
出 处:《中华麻醉学杂志》2010年第8期931-934,共4页Chinese Journal of Anesthesiology
摘 要:目的 评价瑞芬太尼后处理对CPB心内直视手术患者心肌缺血再灌注损伤的影响.方法 择期行室间隔缺损修补术和/或房间隔缺损修补术的先天性心脏病患者30例,年龄18~45岁,ASA分级Ⅱ或Ⅲ级,心功能分级Ⅰ或Ⅱ级,随机分为2组(n=15).在主动脉开放前8 min瑞芬太尼组(R组)从主动脉根部以4μg·kg-1·min-1的速率输注瑞芬太尼5 min,对照组(C组)给予等容量生理盐水.于麻醉诱导前(基础状态)、主动脉开放后4、8、24、48 h时采集右颈内静脉血样,检测心肌肌钙蛋白I(cTnI)、丙二醛(MDA)的浓度及MB型肌酸激酶同工酶(CK-MB)、超氧化物歧化酶(SOD)的活性.结果 与C组比较,R组主动脉开放后4、8 h时cTnI、MDA浓度及CK-MB活性降低,SOD活性升高,主动脉开放后24 h时MDA浓度降低(P<0.05).结论 瑞芬太尼后处理可减轻CPB心内直视手术患者心肌缺血再灌注损伤,其机制与抑制脂质过氧化反应有关.Objective To evaluate the effect of remffentanil postconditioning on myocardial ischemiareperfusion (I/R) injury in patients undergoing open heart surgery under CPB.Methods Thirty patients (ASA grade Ⅱ or Ⅲ, NYHA class Ⅰ or Ⅱ ) of both sexes aged 18-45 yr undergoing repair: of ventricular septal defect and/or atrial septal defect under CPB were randomly divided into 2 groups ( n = 15 each): control group (group C)and remifentanil postconditioning group (group R). Anesthesia was induced with midazolam, sufcntanil, propofol and rocuronium. The patients received 5 min infusion of remifentanil at 4 μg · kg- 1 · min - 1 8 min before aortic unclamping in group R, while the patients received equal volume of normal saline in group C. Blood samples were obtained from the right internal jugular vein for determination of plasma concentrations of cardiac troponin-I (cTnI)and MDA and activities of CK-MB and SOD before induction of anesthesia (baseline) and at4, 8, 24 and48 h after aortic unclamping. Results The plasma concentrations of cTnI and MDA and activity of CK-MB were significantly lower, while the plasma SOD activity was significantly higher at 4 and 8 h after aortic unclmping, and the plasma concentration of MDA was significantly lower at 24 h after aortic unclamping in group R than in group C ( P < 0.05 ). Conclusion Remifentanil postconditioning can attenuate myocardial I/R injury in patients undergoing open heart surgery under CPB through inhibiting lipid peroxidation.
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