盐酸甲氯芬酯对急性一氧化碳中毒患者的疗效及血清氧自由基的影响研究

Effects and Therapeutic Analysis of Meclofenoxate Hydrochloride on the Serum Levels of SOD,GSH-PX and MDA in Patients with Acute Carbon Monoxide Poisoning

目的观察盐酸甲氯芬酯治疗急性一氧化碳中毒患者的疗效并探讨其可能的作用机制。方法将72例急性一氧化碳中毒患者随机分为治疗组与对照组各36例,对照组给予常规治疗及高压氧治疗。治疗组在常规治疗及高压氧治疗基础上加用盐酸甲氯芬酯,0.5g/d,1次/d,静脉滴注,连用14d。分别于治疗前及治疗后3、7、14d检测血清中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)的活性和丙二醛(MDA)的含量,并观察临床症状及体征变化。结果治疗前两组血清SOD、GSH-PX和MDA水平比较差异无统计学意义(P>0.05)。经治疗后,两组血清GSH-PX及SOD水平明显高于治疗前,血清MDA水平低于治疗前。治疗组血清GSH-PX及SOD水平明显高于对照组,血清MDA水平明显低于对照组。治疗组有效率高于对照组。结论盐酸甲氯芬酯对一氧化碳中毒患者有明显临床疗效,并有清除氧自由基作用,抑制脂质过氧化反应,减轻氧自由基对脑细胞的损伤,改善一氧化碳中毒患者的预后。

Objective To investigate the curative effects of meclofenoxate hydrochloride on the treatment of acute carbon monoxide poisoning （ACOP） and to study the mechanisms of its effects. Methods 72 cases of ACOP were randomly divided into two groups, control group and treatment group of 36 cases. The basic treatments of two groups were treated with conven- tional therapy and hyperbaric oxygen treatment. Based on the basic treatments, treatmeat group was treated with meclofenoxate hydrochloride 0. 5g/d, intravenously for 14 days. The serum level of superoxide dismutase （SOD）, glutathione peroxidase （ GSH - PX） and malondialdehyde （MDA） were measured in two groups before treatment and 3, 7, 14d after the treatment, respectively, the vital signs and clinical symptoms were also assessed. Results The serum level of SOD, GSH - Px and MDA in the two groups had no significant differences before treatment （ P 〉 0. 05 ）. The serum level of SOD and GSH - Px in two groups were significantly higher after treatment. The serum level of MDA was lower than that before treatment. After treatment the serum level of SOD and GSH - Px in the treatment group was much higher than that in control group. The serum level of MDA in the treatment group was much lower than that in control group. The effective power of treatment group was higher than that of control group. Conclusion Meclofenoxate hydrochloride could obviously improve the clinic therapeutic effect of ACOP, eliminate oxygen free radical, inhibit lipid peroxidation, decrease the injury of brain cells by oxyradical and improve the prognosis of ACOP.