Willette R N, Krieger A J, Sapru H N
Eur J Pharmacol. 1982 May 7;80(1):57-63. doi: 10.1016/0014-2999(82)90177-7.
[D-Ala2,Met5]enkephalinamide (DAME), [D-Ala2,Leu5]enkephalinamide (DALE) and morphine sulfate (MS) increase activity in the recurrent laryngeal nerve (RLN) within 1 s subsequent to right atrial administration. The activation of the RLN was correlated with a large increase in the resistance to airflow in the in situ isolated larynx. Single unit recurrent laryngeal motoneuron recordings showed that the increase in laryngeal resistance was caused by the continuous activation and recruitment of expiratory motoneurons. Results obtained with opioids mimicked those of phenyldiguanide (20-40 micrograms/kg RA), an agent known to stimulate pulmonary J-receptors. Opioid-induced increases in laryngeal resistance were blocked by bilateral section of the RLN and pretreatment with naloxone (100 micrograms/kg RA). Naloxone had no effect on PDG responses. During the initial period of laryngeal motoneuron activation, the phrenic nerve (PN) was inhibited, however, the activation of the RLN was not dependent upon PN inhibition. It was concluded that stimulation of pulmonary opiate receptors, which may be associated with vagal afferents, elicit a reflex activation of expiratory recurrent laryngeal motoneurons resulting in an increase in laryngeal resistance.
[D-丙氨酸2，蛋氨酸5]脑啡肽酰胺（DAME）、[D-丙氨酸2，亮氨酸5]脑啡肽酰胺（DALE）和硫酸吗啡（MS）在经右心房给药后的1秒内可增加喉返神经（RLN）的活性。RLN的激活与原位分离喉部气流阻力的大幅增加相关。单单位喉返运动神经元记录显示，喉部阻力的增加是由呼气运动神经元的持续激活和募集引起的。使用阿片类药物获得的结果与苯基双胍（20 - 40微克/千克右心房给药）相似，苯基双胍是一种已知可刺激肺J感受器的药物。阿片类药物引起的喉部阻力增加可通过双侧切断RLN和用纳洛酮（100微克/千克右心房给药）预处理来阻断。纳洛酮对苯基双胍的反应没有影响。在喉运动神经元激活的初始阶段，膈神经（PN）受到抑制，然而，RLN的激活并不依赖于PN的抑制。得出的结论是，刺激可能与迷走神经传入相关的肺阿片受体，会引发呼气性喉返运动神经元的反射性激活，导致喉部阻力增加。
