TRH对失血性休克狗脑脊液和血浆ir－β－EP含量的影响

Changes of Immunoreactive Beta-endorphin in Cerebrospinal Fluid and Plasma Induced by Thyrotropin-releasing Hormone during Therapy of Canine Severe Hemorrhagic Shock

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。

Immunoreactive beta-endorphin(ir-β-EP) concentrations in cerebrospinal fluid (CSF) and plasma of dogs were tested simultaneously with and without thyrotropin -releasing hormone (TRH) during severe hemorrhagic shock. The results displayed that CSF and plasma levels of ir-β-EP after shock increased significantly and correlated remarkably with decrease of mean artery pressure,indicating that β-EP in both the central nervous system and circulation was involved in the pathophysiological changes of hemorrhagic shock. CSF and plasma levels of ir-β-EP after in TRH were decreased to those before shock and there were a significant difference as compared with the control group. The fact that TRH suppressed the release of β-EP from hypothalamus and pituitary may be considered as one of the mechanisms of TRH for antishock.