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我们曾证明氯胺酮引起的外周镇痛作用与阿片受体的激活有关。本实验旨在建立吗啡外周镇痛耐受的大鼠模型，进一步观察氯胺酮的外周镇痛作用与阿片受体的关系。外周感受野局部皮下注射５μｌ吗啡（１０μｇ／μｌ），明显的抑制伤害性肌电反应。随吗啡注射次数的增加，伤害性反应的抑制逐渐减弱，一般于第五次注射后，吗啡不再产生抑制，出现外周镇痛的急性耐受。但是，在耐受动物的同一部位注射２０μｌ氯胺酮（５０μｇ／μｌ），仍产生很强的镇痛作用。本结果表明，１．大鼠吗啡外周镇痛的急性耐受，是研究阿片耐受的一种较简便的模型；２．氯胺酮的外周镇痛效应中，除了阿片受体参与外，还有其它不产生耐受的机制。
We have shown that ketamine-induced peripheral analgesia is associated with activation of opioid receptors. The purpose of this study was to establish a rat model of analgesic tolerance to morphine peripheral and to further investigate the relationship between peripheral analgesic effects of ketamine and opioid receptors. Peripheral receptive field local subcutaneous injection of 5μl of morphine (10μg / μl), significantly inhibited the nociceptive response. With the increase of the number of morphine injection, the inhibition of nociceptive response gradually weakened. Generally, after the fifth injection, morphine no longer inhibited and acute tolerance of peripheral analgesia occurred. However, injection of 20 μl of ketamine (50 μg / μl) in the same site of the tolerated animals still produced a strong analgesic effect. The result shows that: 1. Acute tolerance of morphine to peripheral analgesia in rats is a relatively simple model for the study of opiate tolerance; 2. In the peripheral analgesic effect of ketamine, besides the opioid receptor, there are other mechanisms that do not produce tolerance.