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采用狗重度失血性休克模型，同时动态测定了休克及应用促甲状腺素释放激素（ＴＲＨ）后，狗脑脊液（ＣＳＦ）和血浆的β－内啡肽样免疫活性物质（ｉｒ－β－ＥＰ）含量变化。结果显示：失血性休克时ＣＳＦ和血浆ｉｒ－β－ＥＰ含量明显升高，与休克严重程度显著相关。提示中枢神经系统和外周血循环中的β－ＥＰ共同参与失血性休克的病理生理过程。静脉滴注ＴＲＨ后，ＣＳＦ和血浆中的ｉｒ－β－ＥＰ均降到休克前水平，与对照组比较相差显著。ＴＲＨ抑制了下丘脑和垂体释放β－ＥＰ，可能是ＴＲＨ拮抗失血性休克的机理之一。
Severe hemorrhagic shock model was used in dogs, and the content of β-endorphin-like immunoreactive substance (ir-β-EP) in cerebrospinal fluid (CSF) and plasma of dogs was measured after shock and application of TRH Variety. The results showed that the contents of CSF and plasma ir-β-EP in hemorrhagic shock were significantly increased, which were significantly correlated with the severity of shock. It is suggested that the β-EP in the central nervous system and peripheral blood circulation participate in the pathophysiological process of hemorrhagic shock. Intravenous drip TRH, CSF and plasma ir-β-EP were reduced to the level before shock, compared with the control group, a significant difference. TRH inhibits the release of β-EP in the hypothalamus and pituitary, which may be one of the mechanisms by which TRH antagonizes hemorrhagic shock.