Yuge O, Kitahata L M, Collins J G, Matsumoto M, Tabatabai M, Suzukawa M, Tanaka A
Anesth Analg. 1985 Jun;64(6):597-600.
The effects of intravenously administered fentanyl (25 micrograms/kg, n = 9; 50 micrograms/kg, n = 5) and alfentanil (12.5 micrograms/kg, n = 5; 25 micrograms/kg, n = 7) on the noxiously evoked, single-unit activity of cells in the nucleus reticularis gigantocellularis (NRGC) were studied in decerebrate cats. Only cells of the NRGC excited exclusively by supramaximal electrical stimulation of A delta fibers (noxious stimulation) of the superficial radial nerve were studied. The noxiously evoked activity of all cells in the NRGC was suppressed by the administration of opioids (by 58 and 88% for fentanyl, 25 micrograms/kg and 50 micrograms/kg, respectively; by 35 and 78% for alfentanil 12.5 micrograms/kg and 25 micrograms/kg, respectively). Fentanyl and alfentanil effects were antagonized by the intravenous administration of naloxone. These results indicate that opioid suppression of noxiously evoked activity is seen in neurons located in the brainstem, and thus suppression of brainstem neurons may be important in the production of fentanyl and alfentanil analgesia.
在去大脑猫中研究了静脉注射芬太尼（25微克/千克，n = 9；50微克/千克，n = 5）和阿芬太尼（12.5微克/千克，n = 5；25微克/千克，n = 7）对巨细胞网状核（NRGC）中细胞有害刺激诱发的单单位活动的影响。仅研究了由桡神经浅支Aδ纤维的超强电刺激（有害刺激）唯一激发的NRGC细胞。给予阿片类药物可抑制NRGC中所有细胞的有害刺激诱发活动（芬太尼25微克/千克和50微克/千克分别抑制58%和88%；阿芬太尼12.5微克/千克和25微克/千克分别抑制35%和78%）。静脉注射纳洛酮可拮抗芬太尼和阿芬太尼的作用。这些结果表明，在脑干中的神经元中可见阿片类药物对有害刺激诱发活动的抑制，因此抑制脑干神经元可能在芬太尼和阿芬太尼镇痛作用的产生中起重要作用。
