Effects of central chemical drive on poststimulatory respiratory depression of laryngeal origin in the adult cat.

We investigated the influences of central CO2-related chemosensory drive on poststimulatory respiratory phenomena induced by superior laryngeal nerve (SLN) stimulation in pentobarbitone-anesthetized, vagotomized, carotid sinus-denervated, paralyzed, and artificially ventilated adult cats. Respiratory output was monitored as integrated phrenic nerve activity. Under eucapnic conditions, apnea-producing SLN stimulations of both short (10 s) and long (30 s) duration were followed by persistent apnea and depression in phrenic motor output; the latter showed a gradual recovery that followed an exponential time course. Hypocapnia increased the duration of poststimulatory apnea and the intensity of poststimulatory depression in phrenic minute output owing to changes in peak phrenic activity. Hypercapnia did not affect the duration of poststimulatory apnea, but markedly attenuated poststimulatory depression in respiratory activity, mainly due to changes in respiratory frequency. The rate of respiratory recovery was similar under eucapnic and hypocapnic conditions, but it was slower during hypercapnia. The results provide evidence that central chemosensitivity plays a prominent role in counteracting poststimulatory depressant effects on respiration induced by SLN stimulation.