Regulation of ventilatory responses in vagotomized cats by caudal brainstem sites.

Respiratory responses to hypercapnia and isocapnic hypoxia were evaluated in vagotomized decerebrate cats prior to and following lesions in the midline at the pontomedullary junction. Subsequent to these lesions, frequency responses to hypercapnia were significantly elevated whereas the concomitantly determined tidal volumes were significantly lowered. In the post-lesion phase, the durations of inspiration, expiration and the total respiratory cycle at maximum hypercapnia-induced tidal volumes were lower than comparable values at maximum tidal volumes in the pre-lesion phase. The same lesions produced no significant alteration of respiratory responses to hypoxia. Mesencephalic or rostral pontile lesions caused no systematic changes in either hypercapnia- or hypoxia-induced responses. It is concluded that the lesions at the pontomedullary junction produce ventilatory alterations by interrupting a pathway interconnecting the caudal pontile apneustic center with the medullary respiratory complex. The possibility that this interruption produces an alteration in the threshold of the inspiratory off-switch mechanism of the brainstem respiratory controller is considered and discussed.