长期饮酒对异丙酚使患者意识消失的半数有效效应室靶浓度的影响

目的 拟通过探讨长期饮酒对异丙酚使患者意识消失的半数有效效应室靶浓度(EC50)的影响,评价长期饮酒对异丙酚镇静效力的影响.方法 择期拟行外科手术的男性患者50例,年龄25～60岁,体重50～80kg,ASA分级Ⅰ或Ⅱ级,根据是否有长期饮酒史分为2组(n=25),对照组:日饮酒量＜25 g;长期饮酒组:日饮酒量超过45 g持续2年或2年以上.采用序贯法确定异丙酚使患者意识消失的EC50其95%可信区间,长期饮酒组和对照组异丙酚初始效应室靶浓度分别为2.0和1.5μg/ml,各相邻靶浓度之比为1.05.以睫毛反射消失及对言语指令无反应作为判断意识消失的标准.结果 长期饮酒组和对照组异丙酚使患者意识消失时的EC50及其95%可信区间分别为3.92(3.56～4.63)g/ml和2.73(2.26～3.31)μg/ml,长期饮酒组EC50高于对照组(P＜0.05).结论 长期饮酒可增加异丙酚使患者意识消失时的EC50,降低其镇静效力.

Abstract：

Objective To evaluate the effect of chronic alcohol intake on the sedative potency of propofol through investigating the effect of chronic alcohol intake on the half-effective target effect-site concentration ( EC50 )of propofol required for loss of consciousness in patients. Methods Fifty male ASA Ⅰ or Ⅱ patients, aged 25-60 yr, weighing 50-80 kg, scheduled for elective surgery, were divided into 2 groups according to the history of chronic alcoholic intake ( n = 25 each): control group (alcoholic intake per day ＜ 25 g) and chronic alcoholic group (alcoholic intake per day＞45 g, lasting for 2 yr or more). The EC50 and 95% confidence interval (CI)were determined by up-and-down sequential method. The initial target effect-site concentration was 2 μg/nl in chronic alcoholic group and 1.5μg/ml in control group, and the ratio between the two successive concentrations was 1.05. Loss of consciousness was defined as loss of response to verbal command and eyelash stimulation. Results The EC50 of propofol that produced loss of consciousness was 3.92 (95 % CI 3.56-4.63 ) μg/ml in chronic alcoholic group and 2.73 (95%CI 2.26-3.31)μg/ml in control group. The EC50 of propofol was significantly higher in chronic alcoholic group than in control group ( P ＜ 0.05). Conclusion Chronic alcohol intake can increase the EC50 of propofol required to induce loss of consciousness and reduce sedative potency in patients.

Effect of chronic alcohol intake on half- effective target effect- site concentration of propofol required for loss of consciousness

Objective To evaluate the effect of chronic alcohol intake on the sedative potency of propofol through investigating the effect of chronic alcohol intake on the half-effective target effect-site concentration ( EC50 )of propofol required for loss of consciousness in patients. Methods Fifty male ASA Ⅰ or Ⅱ patients, aged 25-60 yr, weighing 50-80 kg, scheduled for elective surgery, were divided into 2 groups according to the history of chronic alcoholic intake ( n = 25 each): control group (alcoholic intake per day ＜ 25 g) and chronic alcoholic group (alcoholic intake per day＞45 g, lasting for 2 yr or more). The EC50 and 95% confidence interval (CI)were determined by up-and-down sequential method. The initial target effect-site concentration was 2 μg/nl in chronic alcoholic group and 1.5μg/ml in control group, and the ratio between the two successive concentrations was 1.05. Loss of consciousness was defined as loss of response to verbal command and eyelash stimulation. Results The EC50 of propofol that produced loss of consciousness was 3.92 (95 % CI 3.56-4.63 ) μg/ml in chronic alcoholic group and 2.73 (95%CI 2.26-3.31)μg/ml in control group. The EC50 of propofol was significantly higher in chronic alcoholic group than in control group ( P ＜ 0.05). Conclusion Chronic alcohol intake can increase the EC50 of propofol required to induce loss of consciousness and reduce sedative potency in patients.