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目的和方法：用兔侧脑室给药观察了δ亚型阿片受体拮抗剂ＩＣＩ１７４，８６４和κ亚型阿片受体特异性拮抗剂ｎｏｒ－ｂｉｎａｌｔｏｒｐｈｉｍｉｎｅ（Ｎｏｒ－ＢＮＴ）预处理对促甲状腺素释放激素（ＴＲＨ）抗休克作用的影响。结果：ＴＲＨ（５０μｇ，ｉｃｖ）可明显升高失血性休克兔平均动脉压（ＭＡＰ），左室收缩压（ＬＶＳＰ），改善失血性休克心肌收缩力指标如心室内压最大上升和下降速率（±ｄｐ／ｄｔｍａｘ），心肌纤维收缩速度（Ｖｃｅ４０，Ｖｐｍ）和心肌收缩向量环面积（Ｌｏ）。δ－亚型阿片受体特异拮抗剂ＩＣＩ１７４，８６４预处理可取消ＴＲＨ的上述作用，κ－亚型阿片受体特异拮抗Ｎｏｒ－ＢＮＴ预处理不能取消ＴＲＨ的作用。结论：ＴＲＨ的抗休克作用与δ－亚型阿片受体有关，与κ－亚型阿片受体关系不大
PURPOSE AND METHODS: The effects of preconditioning of δ-subtype opioid receptor antagonist ICI174,864 and nor-binaltorphimine (Nor-BNT), a specific antagonist of κ subtype opioid receptor, on thyrotropin-releasing hormone (TRH) anti-shock effect. Results: TRH (50μg, icv) could significantly increase mean arterial pressure (MAP) and left ventricular systolic pressure (LVSP) in hemorrhagic shock rabbits and improve myocardial contractility index of hemorrhagic shock such as the maximal increase and decrease rate of dp / dtmax), myocardial fiber contraction velocity (Vce40, Vpm) and myocardial systolic vector annulus (Lo). Pretreatment with δ-subunit opioid receptor ICI174,864 abolished the above-mentioned effects of TRH. The specific antagonism of κ-subtype opioid receptor by Nor-BNT pretreatment can not cancel the effect of TRH. Conclusion: The anti-shock effect of TRH is related to δ-subtype opioid receptor but not to κ-subtype opioid receptor