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给♂ＳＤ大鼠颈动脉放血，使平均动脉压维持在６．６７ｋＰａ水平，形成出血性休克。从颈静脉给予不同阿片肽拮抗剂：β－内啡肽抗血清（１：３００００，１０μｌ）；β－ＦＮＡ（２ｍｇ）或促甲状腺素释放激素（ＴＲＨ，２ｍｇ），并在随后１、２、３ｈ再给予上述剂量的半量。观察对出血性休克的影响。结果表明：β－内啡肽抗血清可回升动物血压，延缓心率的下降，改善血液生化指标，作用较持久，并可延长休克动物的存活时间；β－ＦＮＡ一定程度上改善休克动物的血压、心率和血液生化指标。ＴＲＨ对休克动物的血压有显著的提升作用，对心率也有延缓下降的作用，但作用短暂，后期心血管功能下降加快。这表明内源性阿片肽参与出血性休克，从不同层次拮抗其作用，有不同程度的抗休克效果，而以直接对抗β－内啡肽的抗休克效果最为明显。
To ♂ SD rat carotid bleeding, the average arterial pressure maintained at 6.67kPa level, the formation of hemorrhagic shock. Different opioid antagonists were administered from the jugular vein: β-endorphin antiserum (1: 30000, 10 μl); β-FNA (2 mg) or thyrotropin releasing hormone (TRH, 2 mg) 3h and then given the dose of half the amount. To observe the impact of hemorrhagic shock. The results showed that β-endorphin antiserum could elevate the blood pressure of animals, delay the decrease of heart rate, improve the blood biochemical indexes, prolong the survival time and prolong the survival time of shock animals. Β-FNA can improve the blood pressure of shock animals to a certain extent, Heart rate and blood biochemical indicators. TRH can significantly improve the blood pressure of shocked animals, but also slow down the heart rate. However, the effect of TRH is transient and the decline of cardiovascular function is accelerated in the later period. This indicates that endogenous opioid peptide is involved in hemorrhagic shock and antagonizes its effects at different levels, with varying degrees of anti-shock effects, whereas the direct anti-shock effects of β-endorphin are the most obvious.