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目的：研究阿片受体阻断剂纳洛酮抗急性失血性休克的外周作用机制．方法和结果：麻醉兔急性失血性休克时，肾交感神经活动和心率分别抑制４１．１±１０．２％和１７．９±６．４％；切断双侧迷走神经，可以翻转此抑制现象；先切断迷走神经后急性失血，此抑制现象消失．急性失血并切断迷走神经后，静脉注射纳洛酮（１ｍｇ／ｋｇ）仍可使血压显著回升，但对肾交感神经活动和心率无明显影响．静脉注射纳洛酮并不能阻断急性失血性休克时肾交感神经和心率的抑制现象．结论：急性失血性休克时肾交感神经活动和心率均受到抑制．纳洛酮对抗失血性休克的重要途径是通过对外周血管的作用．
OBJECTIVE: To study the peripheral mechanism of naloxone, an opioid receptor blocker, against acute hemorrhagic shock. Methods and Results: Renal sympathetic nerve activity and heart rate were 41.1 ± 10.2% and 17.9 ± 6.4%, respectively, in anesthetized rabbits with acute hemorrhagic shock. The bilateral vagus nerve was cut off and the inhibitory effect could be reversed. After cutting off the vagal nerve acute blood loss, this inhibition disappeared. After acute blood loss and vagotomy, intravenous injection of naloxone (1 mg / kg) still markedly increased blood pressure, but had no significant effect on renal sympathetic nerve activity and heart rate. Intravenous naloxone did not block renal sympathetic and heart rate suppression during acute hemorrhagic shock. CONCLUSION: Renal sympathetic nerve activity and heart rate are all inhibited in acute hemorrhagic shock. Naloxone is an important way to combat hemorrhagic shock by acting on peripheral blood vessels.