Zuniga J, Joseph S, Knigge K
Neuroendocrine Unit, University of Rochester, NY 14642.
Eur J Pharmacol. 1987 Oct 6;142(1):51-60. doi: 10.1016/0014-2999(87)90653-4.
Analgesia induced by nitrous oxide was examined using radiant heat tail flick and electrical evoked foot flick tests in rats. Rats exposed to 80 and 60% nitrous oxide expressed statistically significant elevations of percent analgesia (% MPE) compared to air exposed rats. Rats exposed to 30% nitrous oxide showed no significant difference in percent analgesia. Pretreatment with naloxone (10 mg/kg s.c.) produced a significant decrease in %MPE and an increase in variance of response after exposures to 80% nitrous oxide in a double blind study. Kainic acid lesions of the ventral and caudal periaqueductal grey (PAG) reversed analgesia produced by 80% nitrous oxide in a crossover blink study compared to saline lesions. In conclusion, this evidence suggests that the caudal-PAG-raphe mangus-dorsal horn pain inhibition pathway is in part involved in the analgesia induced by nitrous oxide.
使用辐射热甩尾和电刺激诱发足部甩尾试验，在大鼠中检测氧化亚氮诱导的镇痛作用。与暴露于空气的大鼠相比，暴露于80%和60%氧化亚氮的大鼠在镇痛百分比（%MPE）上有统计学显著升高。暴露于30%氧化亚氮的大鼠在镇痛百分比上无显著差异。在一项双盲研究中，用纳洛酮（10mg/kg皮下注射）预处理后，暴露于80%氧化亚氮的大鼠的%MPE显著降低，反应变异性增加。在一项交叉眨眼研究中，与生理盐水损伤相比，腹侧和尾侧导水管周围灰质（PAG）的 kainic 酸损伤逆转了80%氧化亚氮产生的镇痛作用。总之，该证据表明，尾侧-PAG-中缝大核-背角疼痛抑制通路部分参与氧化亚氮诱导的镇痛作用。
