Waldrop T G, Eldridge F L, Millhorn D E
Respir Physiol. 1983 Nov;54(2):211-22. doi: 10.1016/0034-5687(83)90058-0.
Stimulation of receptors in hindlimb muscles activates a supraspinal mechanism which causes a prolonged, post-stimulatory depression of breathing (Waldrop, T.G., F.L. Eldridge and D.E. Millhorn, 1982, Respir. Physiol. 50: 239-254). In the present study phrenic nerve responses to stimulation of hindlimb muscles were studied in anesthetized, paralyzed cats whose vagi and carotid sinus nerves had been cut. Body temperature and end-tidal PCO2 were kept constant with servocontrollers. The post-stimulatory depression of breathing was greatly attenuated in cats pretreated with an opiate antagonist (naloxone) and did not occur in animals pretreated with a GABA antagonist (bicuculline). The response was not blocked by prior administration of either a serotonin antagonist (methysergide) or a dopamine and norepinephrine antagonist (alpha-methyltyrosine). We conclude that endogenous opiates and possibly GABA, but not serotonin, dopamine or norepinephrine, are involved in the neural mechanism responsible for the prolonged depression of breathing.
刺激后肢肌肉中的感受器会激活一种脊髓上机制，该机制会导致呼吸出现长时间的刺激后抑制（Waldrop, T.G., F.L. Eldridge和D.E. Millhorn, 1982年，《呼吸生理学》50: 239 - 254）。在本研究中，在麻醉、麻痹且迷走神经和颈动脉窦神经已被切断的猫身上，研究了膈神经对后肢肌肉刺激的反应。通过伺服控制器使体温和呼气末PCO2保持恒定。在用阿片类拮抗剂（纳洛酮）预处理的猫中，呼吸的刺激后抑制大大减弱，而在用GABA拮抗剂（荷包牡丹碱）预处理的动物中未出现这种抑制。预先给予5-羟色胺拮抗剂（麦角新碱）或多巴胺和去甲肾上腺素拮抗剂（α-甲基酪氨酸）均不能阻断该反应。我们得出结论，内源性阿片类物质以及可能的GABA，但不是5-羟色胺、多巴胺或去甲肾上腺素，参与了导致呼吸长时间抑制的神经机制。
