纳洛酮对心搏骤停患者心肺复苏后氧化应激反应及缺血缺氧性脑病的影响

Effects of Naloxone on Oxidative Stress and Hypoxic-ischemic Encephalopathy after Cardio-pulmonary Resuscitation in Patients with Cardiac Arrest

目的：探讨纳洛酮对心搏骤停患者心肺复苏（CPR）后氧化应激反应及缺血缺氧性脑病的影响。方法：将我院收治的78例骤停时间≤10 min的心搏骤停患者随机分为治疗组和对照组,每组各39例。两组均按照美国心脏学会心肺复苏指南进行标准的心肺复苏,治疗组在此基础上静脉注射纳洛酮2 mg,复苏后用纳洛酮0.4 mg/（kg·d）微量注射泵24h持续泵入。比较两组的CPR成功率、血浆丙二醛（MDA）含量和谷胱甘肽过氧化物酶（GSH-PX）、超氧化物歧化酶（SOD）活性,监测其不同时点脑氧摄取量（CEO2）的变化。结果：与对照组比较,治疗组自主循环恢复成功率、复苏后24 h存活率均显著升高（P〈0.05）。自主循环恢复后,治疗组SOD、GSH-PX活性较对照组明显增加（P〈0.05）;复苏后24 h,两组MDA含量均显著升高,SOD、GSH-PX活性明显减弱,而治疗组各氧化应激指标明显优于对照组（P〈0.05）。两组患者在复苏早期CEO2迅速升高,但在复苏后24 h开始下降,48~72 h处于相对稳定的水平,治疗组各时间点CEO2均明显高于对照组（P〈0.05）。结论：纳洛酮可减轻心搏骤停患者CPR后体内氧化应激损伤和缺血缺氧性脑病,改善患者的预后。

Objective： To investigate the clinical efficacy of naloxone on oxidative stress and hypoxic-ischemic encephalopathy after cardio-pulmonary resuscitation（CPR） in patients with cardiac arrest. Methods： 78 patients suffered cardiac arrest with 10 min were selected and randomly divided into treatment group and control group, 39 cases in each group. Standard CPR according to AHA guidelines were practiced immediately in both groups. Moreover, patients in treatment group were additionally given naloxone intravenous injection for 2 mg, and 0.4 mg/（kg·d） using micro-infusion pump for 24 h after resuscitation. The content of plasma malondialdehyde（MDA）, the activity of glutathione peroxidase（GSH-PX） and superoxide dismutase（SOD） were detected, and cerebral extraction of oxygen（CEO2） at different time points were detected and compared between the two groups. Results： The successful rate of restoration of spontaneous circulation（ROSC）, 24 h survival rate after CPR of treatment group were both remarkably higher compared with those of the control group（P0.05）. After ROSC, the activity of GSH-PX and SOD were strengthened in the treatment group than those in the control group（P0.05）. At 24 h after CPR, the content of MDA increased, activity of SOD and GSH-PX were significantly decreased in both groups（P0.05）, while all the levels of oxidative stress index in treatment group were significantly better than those in the control group（P0.05）. The CEO2 rose rapidly in the early phase of CPR, and began to decline at 24 h after CPR, turn to a relatively stable level at 48~72 h after CPR in both groups. The CEO2 at all different time points in the treatment group were higher than those in the control group（P0.05）. Conclusion： Naloxone could effectively relieve the oxidative stress and hypoxic-ischemic encephalopathy after CPR in patients with cardiac arrest and improve the prognosis.