Opioids increase laryngeal resistance and motoneuron activity in the recurrent laryngeal nerve

Robert N. Willette, A. J. Krieger, H. N. Sapru

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

[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 phenydiguanide (20-40 μg/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 μg/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.

Original languageEnglish (US)
Pages (from-to)57-63
Number of pages7
JournalEuropean Journal of Pharmacology
Volume80
Issue number1
DOIs
StatePublished - May 7 1982

All Science Journal Classification (ASJC) codes

  • Pharmacology

Keywords

  • Laryngeal motoneurons
  • Laryngeal resistance
  • Opioids
  • Pulmonary chemoreflex
  • Pulmonary opiate receptors
  • Type J receptors
  • Vagovagal reflex

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