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目的：研究动脉壁阿片受体参与休克时血管机能的调节；方法：作者使用大鼠失血性休克模型和离体动脉条灌流，研究动脉壁阿片受体在休克时血管机能调节中的作用。结果：造成失血使大鼠血压下降并维持在３．９９ｋＰａ，纳洛酮组平均最大失血量为２５．９０±４．２３ｍｌ／ｋｇ，对照组为２０．２６±４．４３ｍｌ／ｋｇ，相差显著（Ｐ＜０．０５）；纳洛酮组的休克血管收缩期为５０．００±１１．５３ｍｉｎ，对照组为３１．８８±９．９８ｍｉｎ，相差亦显著（Ｐ＜０．０５）．电场刺激离体灌流的胸主动脉条，发现休克组动脉条收缩反应明显小于正常对照组，给予纳洛酮（１．３７×１０￣（－５）ｍｏｌ／Ｌ）后，休克组动脉条收缩反应的增强率则显著高于对照组（Ｐ＜０．０１）．结论：失血性休克时动脉收缩机能的下降有阿片受体参与作用；纳洛酮可直接作用于动脉壁上的阿片受体，阻断阿片肽对血管收缩的抑制作用，从而起升高血压对抗休克的作用．
OBJECTIVE: To study the regulation of arterial wall opioid receptors involved in the regulation of vascular function in shock. Methods: Using the rat hemorrhagic shock model and isolated arterial strip perfusion, we investigated the role of arterial wall opioid receptors in the regulation of vascular function during shock. Results: Blood loss caused by blood loss decreased to 3.99kPa in rats. The average blood loss in naloxone group was 25.90 ± 4.23ml / kg, while that in control group was 20.26 ± 4.43ml / kg, with a significant difference (P <0.05). The nausea and vasoconstriction of naloxone group were 50.00 ± 11.53min and 31.88 ± 9.98min, respectively. The difference was also significant (P <0.05). After the electric field stimulated the thoracic aortic strips perfusion in vitro, the contractile response of the aortic strips in shock group was significantly lower than that in the normal control group. After naloxone (1.37 × 10 ~ (-5) mol / L) The response rate was significantly higher than the control group (P <0.01). CONCLUSION: The decline of arterial systolic function during hemorrhagic shock has the function of opioid receptor. Naloxone can act directly on the opioid receptors in the arterial wall and block the inhibitory effect of opioid on vasoconstriction, thus elevating the antihypertensive response The role of shock.