Cowlrick I S, Shepperson N B
Br J Pharmacol. 1985 May;85(1):205-11. doi: 10.1111/j.1476-5381.1985.tb08848.x.
In the conscious rat arterial PCO2 was measured as an index of respiratory status. The opioid analgesic meptazinol (7.5 - 30 mg kg-1) evoked small but significant increases in arterial PCO2 which were attenuated by naloxone. Meptazinol significantly reduced the increase in arterial PCO2 evoked by morphine. The respiratory depression induced by meptazinol, but not that induced by morphine, was enhanced by pretreatment with atropine. The (+)-enantiomer, but not the (-)-enantiomer of meptazinol increased arterial PCO2. In contrast, only the (-)-enantiomer reduced the respiratory depressant effect of morphine. It is proposed that the degree of respiratory depression induced by meptazinol is limited by its opioid antagonist and cholinomimetic properties.
在清醒大鼠中,测量动脉血二氧化碳分压(PCO2)作为呼吸状态指标。阿片类镇痛药美普他酚(7.5 - 30毫克/千克)可引起动脉血PCO2小幅但显著升高,且这种升高可被纳洛酮减弱。美普他酚可显著降低吗啡引起的动脉血PCO2升高。用阿托品预处理可增强美普他酚诱导的呼吸抑制,但不能增强吗啡诱导的呼吸抑制。美普他酚的(+)-对映体可增加动脉血PCO2,而(-)-对映体则不能。相反,只有(-)-对映体可降低吗啡的呼吸抑制作用。有人提出,美普他酚诱导的呼吸抑制程度受其阿片类拮抗剂和拟胆碱特性的限制。