NALOXONE ATTENUATES POSTSTIMULATORY RESPIRATORY DEPRESSION OF LARYNGEAL ORIGIN IN THE ADULT CAT

Poststimulatory depression in respiratory activity induced by superior laryngeal nerve (SLN) stimulation was quantitatively investigated in 20 adult cats. The role played in this phenomenon by endogenous opioid s was studied using the opiate antagonist naloxone. The effects of hyp ercapnia on the same phenomenon were also investigated for comparison. Experiments were performed on cats anesthetized with pentobarbitone o r alpha-chloralose, vagotomized, paralyzed, and artificially ventilate d with 100% O-2. Some animals were also carotid sinus denervated. Resp iratory output was monitored as integrated phrenic nerve activity. SLN stimulation produced apnea, which outlasted the stimulation period; w hen respiration resumed, it was markedly depressed as revealed mainly by a decrease in phrenic minute output, respiratory frequency, and rat e of rise of inspiratory activity. Phrenic output recovered gradually to control levels following an exponential time course. These effects varied as a function of the duration of SLN stimulation. Naloxone admi nistration (0.8 mg/kg iv) significantly reduced the duration of postst imulatory apnea and attenuated the depression of phrenic minute output of the first recovery breath as a result of changes in peak phrenic a ctivity; it also accelerated the time course of recovery. Hypercapnia did not affect the duration of poststimulatory apnea, but attenuated t he initial poststimulatory depression because of changes in respirator y frequency; the rate of recovery was reduced. The results provide cha racterization of poststimulatory respiratory depression of laryngeal o rigin in the adult cat and suggest a role of endogenous opioids in its genesis or modulation.