摘要
目的:探讨三种物质急性中毒患者血清β-内啡肽浓度变化及意义。方法:用放射免疫法测定急性乙醇中毒20例,急性一氧化碳中毒25例,急性镇静催眠药中毒20例共65例患者血清β-内啡肽浓度并与25例健康者进行比较。结果:急性酒精和一氧化碳中毒患者治疗前的β-内啡肽水平显著升高(P<0.001),一氧化碳中毒治疗后24h 持续较高水平(P<0.05);酒精中毒治疗后24hβ-内啡肽水平明显下降(P<0.001);镇静催眠药物中毒患者治疗前、后的β-EP 并不增高(P>0.05)。结论:急性酒精和一氧化碳中毒导致大量释放β-内啡肽,急性镇静催眠药物中毒时β-EP 水平不升高;同时高水平β-内啡肽可导致或参与中毒时脑组织缺血性障碍和脑组织损伤,致继发性脑组织损伤,可能是酒精性脑病的病理机理之一。纳洛酮能拮抗急性酒精和一氧化碳中毒时高水平β-EP从而解除β-EP 对中枢神经的抑制作用,阻断或逆转继发性脑组织损伤;而可能对镇静催眠药物中毒无疗效。
Objective:To investigate the changes of serum β-endorphin and its significance in patients with acute intosication of three kinds in substances.Methods:The serum β-EP concentration was mea- sured by radioimmunoassy poisoning before treatment,24 hours after treatment.Results:The levels of β- EP were significantly increased in the acute alcoholic and carbon monoxide poisoning group before treat- ment(P<0.001).The level of β-EP in the acute alcoholic poisoning group was significantly decreased 24 hours after treatment(P<0.001)and serum β-EP maintain higher level with the acute carbon monoxide poisoning group 24 hours after treatment in comparison with that before treatment respectived(P<0.05) .The levels of β-EP were not significantly changed in the acute sedative-hypnotics poisoning group before treatment and 24 hours after treatment(P>0.05).Concluston:Acute alcoholic and carbon monoxide in- toxication give rise to releasing of β-EP largely,mean while the higher level of β-EP may results in cere- bral ischemic dysfunction and secondary cerebral injury with alcoholic and carbon monoxide poisoning, and the result may be one of the pathological mechanism about alcoholic encephalopathy.Naloxone may have an effect on releasing restricted nerve center and interdict secondary cerebral injury in higher level of β-EP with the acute alcoholic and carbon monoxide poisoning and naloxone has no effect on the acute sed- ative-hypnotics intoxication.
