Paakkari P, Paakkari I, Landes P, Sirén A L, Feuerstein G
Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD 20184.
Neuropharmacology. 1993 Apr;32(4):323-9. doi: 10.1016/0028-3908(93)90152-s.
Interactions of mu-opioid receptors with the benzodiazepine system were studied by examining the modulatory effects of flumazenil (a benzodiazepine antagonist) and alprazolam (a benzodiazepine agonist) on the respiratory effects of the opioid peptide dermorphin. Dermorphin, 1-30 nmol administered i.c.v., to conscious, unrestrained rats decreased ventilation rate (VR) and minute volume (MV) dose-dependently. The ventilatory depression was antagonized by naloxone and by the benzodiazepine antagonist flumazenil. The benzodiazepine alprazolam potentiated the respiratory inhibition of a small (1 nmol) dose of dermorphin but antagonized that of a higher dose (3 nmol). The results suggest that the benzodiazepine/GABA receptor complex modulates respiratory depression induced by central mu-receptor stimulation in the rat.
通过研究氟马西尼(一种苯二氮䓬拮抗剂)和阿普唑仑(一种苯二氮䓬激动剂)对阿片肽德尔吗啡呼吸作用的调节效应,来探讨μ-阿片受体与苯二氮䓬系统的相互作用。给清醒、不受约束的大鼠脑室内注射1-30纳摩尔的德尔吗啡,可剂量依赖性地降低通气率(VR)和分钟通气量(MV)。纳洛酮和苯二氮䓬拮抗剂氟马西尼可拮抗这种通气抑制。苯二氮䓬类药物阿普唑仑可增强小剂量(1纳摩尔)德尔吗啡的呼吸抑制作用,但拮抗大剂量(3纳摩尔)德尔吗啡的呼吸抑制作用。结果表明,苯二氮䓬/GABA受体复合物可调节大鼠中枢μ-受体刺激诱导的呼吸抑制。