Jaros T, Kolasiewicz W
Institute of Pharmacology, Polish Academy of Sciences, Kraków.
Pol J Pharmacol. 1995 Jan-Feb;47(1):19-24.
Fentanyl given in a low dose of 25 microgram/kg (ip) evoked a marked muscle rigidity measured directly by a mechanographic method in non-anesthetized rats. The selective 5HT1A receptor agonist 8-OH-DPAT (0.1, 0.3 and 1.0 mg/kg ip) showed only a tendency to attenuate the natural muscle tone. However, when that compound was given 40 min before (0.3 and 1.0 mg/kg ip) or 20 min after (1.0 mg/kg ip) fentanyl, it abolished the muscle rigidity. It is concluded that the serotonergic transmission, possibly via 5HT1A receptors, may participate in elucidation of the mechanism(s) of the fentanyl-induced muscle rigidity. These results seem to be clinically important in case other 5HT1A agonists, buspirone or gepirone (potent anxiolytics), also prevented fentanyl-induced muscle rigidity in humans.
以25微克/千克的低剂量腹腔注射芬太尼，通过机械记录法直接测量，可诱发未麻醉大鼠出现明显的肌肉强直。选择性5-羟色胺1A（5HT1A）受体激动剂8-羟基二丙胺基四氢萘（8-OH-DPAT，腹腔注射剂量为0.1、0.3和1.0毫克/千克）仅显示出减弱自然肌张力的趋势。然而，当该化合物在芬太尼给药前40分钟（腹腔注射剂量为0.3和1.0毫克/千克）或给药后20分钟（腹腔注射剂量为1.0毫克/千克）给药时，可消除肌肉强直。由此得出结论，5-羟色胺能传递可能通过5HT1A受体，参与阐明芬太尼诱发肌肉强直的机制。如果其他5HT1A激动剂，如丁螺环酮或吉哌隆（强效抗焦虑药）也能预防人体芬太尼诱发的肌肉强直，这些结果在临床上似乎具有重要意义。
