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目的观察急性一氧化碳中毒(ACOP)患者血浆一氧化氮(NO)、内皮素(ET1)含量的变化及纳络酮对其影响。方法选择重度急性一氧化碳中毒(ACOP)患者50例,随机分为高压氧治疗组(对照组)和纳络酮+高压氧治疗组(观察组),采用硝酸还原酶法、放射免疫吸附法,分别检测两组患者治疗前后血浆NO、ET1含量的变化,并与20名健康体检者(正常组)进行对比分析。结果ACOP患者血浆NO含量较正常组显著降低,而ET1含量明显增高(P<0.01);与对照组比较纳络酮治疗后患者血浆中NO升高、ET1降低(P<0.01)。而且纳络酮治疗后患者的昏迷时间明显缩短,病死率和迟发性脑病的发生率明显减少。结论ACOP患者血中NO水平降低和ET1含量升高参与了ACOP的病理生理过程;纳络酮可提高NO水平、降低ET1含量,对NO、ET1含量的变化具有有益的调节作用,可改善ACOP的病理损害作用。
Objective To investigate the changes of plasma nitric oxide (NO) and endothelin (ET1) in patients with acute carbon monoxide poisoning (ACOP) and the effect of naloxone on them. Methods Fifty patients with acute severe acute carbon monoxide poisoning (ACOP) were randomly divided into hyperbaric oxygen therapy group (control group) and naloxone + hyperbaric oxygen therapy group (observation group). Nitric acid reductase method and radioimmunoassay The changes of plasma NO and ET1 levels before and after treatment in both groups were detected and compared with 20 healthy subjects (normal group). Results Compared with the control group, NO level in plasma of patients with ACOP was significantly lower than that of the normal group and ET1 was significantly increased (P <0.01). And naloxone in patients with coma after treatment was significantly shorter, mortality and delayed encephalopathy incidence was significantly reduced. CONCLUSION: The decrease of NO level and the increase of ET1 level in ACOP patients are involved in the pathophysiological process of ACOP. Naloxone can increase the level of NO and decrease the content of ET1, which has a beneficial effect on the changes of NO and ET1 levels, Pathological damage.