大鼠烫伤后下丘脑室旁核β-内啡肽的变化及δ受体的作用

目的　探讨大鼠烫伤后不同时间下丘脑室旁核β 内啡肽水平的变化和阿片δ受体的作用。　方法　在大鼠背部 2 0 %体表面积Ⅲ度烫伤后不同时间 ,采用放射免疫分析法测定下丘脑室旁核 β 内啡肽免疫活性物质含量的变化 ;通过下丘脑室旁核微量注射δ受体激动剂DPDPE或其拮抗剂ICI174 86 4后心功能指标和存活时间的变化 ,探讨δ受体在大鼠烫伤休克中的作用。　结果　 (1)大鼠烫伤后 1、2、4h ,下丘脑室旁核 β 内啡肽免疫活性物质的含量显著升高 (P <0 .0 1) ;(2 )与对照组比较 ,给予ICI174 86 4后不同时间 ,动物平均动脉压、左心室内压最大上升速率与各自伤前基础值的比值显著升高 ,给予DPDPE则显著降低。但无论给予ICI174 86 4或DPDPE ,心率比值的变化相差不显著 ;(3)ICI174 86 4组动物的平均存活时间明显长于DPDPE组 (P <0 .0 1)。　结论　下丘脑室旁核 β 内啡肽的过量增加是促使休克加重和加快死亡的原因之一 ,该处δ受体可能起了重要的介导作用 ;拮抗δ受体的作用有利于对抗烫伤休克 ,延长存活时间。

The postburn change in hypothalamic paraventricular β-endorphin and the roles of δ-receptor in scalded rats

OBJECTIVE: To investigate the postburn change in hypothalamic paraventricular beta-endorphin and the roles of delta-receptor in scalded rats. METHODS: Male Sprague-Dawley (SD) rats were randomly divided into 3 groups, i.e. ICI174864, DPDPE and control groups. The rats were inflicted with 20% TBSA of III degree scalding on the back by boiling (100 degrees ) water. The postburn change in the tissue content of the hypothalamic paraventricular beta-endorphin was determined by radioimmuno assay (RIA). The effects of delta-receptor in scalded shock rats were investigated by observing the change of the rats'survival time and cardiac indices after the micro-injection of delta-receptor agonist DPDPE or antagonist ICI174864 into the hypothalamic paraventricle. RESULTS: (1) The tissue content of the hypothalamic paraventricular beta-endorphin increased significantly (P < 0.01) at 1, 2 and 4 postburn hours (PBHs) in the scalded rats. (2) When compared with that of control group, the ratio of the cardiovascular parameters mean arterial pressure (MAP), dp/dt(max) and HR] were obviously increased at different time points in rats with pre-injection of ICI174864 whereas the ratio was decreased when DPDPE was used. Nevertheless, the change in the heart rate ratio was not obvious whether ICI174864 or DPDPE was used. (3) The average animal survival time in ICI174864 group was much longer than that in DPDPE group. CONCLUSION: An excessive increase in hypothalamic paraventricular beta-endorphin was one of the factors leading to the aggravation of burn shock and earlier death. delta-receptor located in the tissue might have played important roles in the mediation of the action of hypothalamic paraventricular beta-endorphin. It is beneficial to antagonize the action of delta-receptor for the correction of burn shock and for the prolongation of the of life of animals.