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 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.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Willette RN,Krieger AJ,Sapru HNdoi
10.1016/0014-2999(82)90177-7subject
Has Abstractpub_date
1982-05-07 00:00:00pages
57-63issue
1eissn
0014-2999issn
1879-0712pii
0014-2999(82)90177-7journal_volume
80pub_type
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