促甲状腺素释放激素对失血性休克大鼠脑μ、δ和K阿片受体的影响  

Effects of thyrotropin releasing hormone on brain μ-,δ-andk-opioid receptors during hemorrhagic shock in rats

作　　者：刘良明[1] 胡德耀[1] 陈惠孙[1] 卢儒权[1] 李天星[1] 

机构地区：[1]第三军医大学野战外科研究所

出　　处：《中国药理学与毒理学杂志》1995年第4期268-270,共3页Chinese Journal of Pharmacology and Toxicology

基　　金：国家自然科学基金

摘　　要：本文用放射性相对选择性配体初步研究了促甲状腺素释放素（ＴＲＨ）对失血性休克大鼠脑μ、δ和Ｋ阿片受体的影响。结果显示失血性休克大鼠δ和ｋ阿片受体最大结合数（Ｂｍａｘ）显著升高，亲和力变化不大，μ阿片受体Ｂｍａｘ和亲和力无明显变化。ＴＲＨ（５ｍｇ·ｋｇ￣（－１））可使休克大鼠脑δ阿片受体Ｂｍａｘ降低，对其亲和力影响不大，对μ和ｋ受体无明显影响。这一结果提示ＴＲＨ减数调节失血性休克动物脑阿片受体数量可能是ＴＲＨ拮抗内阿片肽的心血管抑制作用，发挥抗休克作用的重要机理。Effects of thyrotropin-releasing hormone(TRH)on brain μ-,δ-and k-opioid receptors in rats sub-jeted to hemorrhagic shock have been investigated by ra-dio-ligand combining test with relatively selective ligands.The results showed that the maximal binding site(B_(max))ofbrain δ-and k-and k-opioid receptor duri ng hemorrhagicshock in rats increased significantly,their affinity did notchange remarkably,while both the B_(max) and the affinityof μ-opioid receptor did not notably aIter.TRH(5 mg·kg-1)could deereased the brain δ-opioid receptor in B_(max)significantly,but it did not influenee its affinity.TRH didnot influence μ-and k-opioid receptor both in B_(max) andaffinity. These results suggest that the down-regulation ofbrain δ-opioid receptor of shock animal may be an impor-ant mechanism by which TRH antagonizes the depressingeffects of endogenous opioid peptides on cardiovascularsystem to reverse shock.

关 键 词：促甲状腺素 释放激素 休克 出血性 受体 内啡肽 

分 类 号：R977.1[医药卫生—药品]