Moody E J, Mattson M, Newman A H, Rice K C, Skolnick P
Laboratory of Neuroscience, NIDDK, Bethesda, MD 20892.
Life Sci. 1989;44(11):703-9. doi: 10.1016/0024-3205(89)90381-0.
The opiate antagonist naloxone was found to block nitrous oxide analgesia in a stereospecific fashion. Using a modified hotplate test in mice, the (-)-enantiomer of naloxone (which has a KD of approximately 1 nM for opiate receptors) antagonized the analgesic actions of nitrous oxide in a dose-dependent (2.5-20 mg/kg) fashion. In contrast, the (+)-enantiomer (KD approximately 10,000 nM) had no effect on nitrous oxide analgesia at the highest dose tested (40 mg/kg). These data strongly suggest that nitrous oxide analgesia is mediated via opiate receptors and is consistent with the hypotheses that this effect occurs either through the release of endogenous opioids or by physical perturbation of the opiate receptors.
已发现阿片拮抗剂纳洛酮能以立体特异性方式阻断一氧化二氮镇痛作用。在对小鼠进行的改良热板试验中，纳洛酮的（-）-对映体（对阿片受体的解离常数KD约为1 nM）以剂量依赖性方式（2.5 - 20 mg/kg）拮抗一氧化二氮的镇痛作用。相比之下，（+）-对映体（KD约为10,000 nM）在测试的最高剂量（40 mg/kg）下对一氧化二氮镇痛无作用。这些数据有力地表明，一氧化二氮镇痛是通过阿片受体介导的，这与该效应通过内源性阿片类物质释放或阿片受体的物理扰动而发生的假设一致。
