Abstract
In spontaneously breathing or paralyzed, ventilated, decerebrate cats, bilateral pneumotaxic center lesions and bilateral vagotomy resulted in apneusis characterized by a marked prolongation of inspiratory duration ( Ti) and, concomitantly, an elevation of tidal volume (V t) and reduction of respiratory frequency (f). Subsequent placement of medial or lateral lesions in the caudal pons or medulla reduced T i and V t, increased f, and restored a more regular rhythmic respiratory pattern. Placement of these pontile or medullary lesions in animals with pneumotaxic center lesions prevented the development of a typical apneustic pattern upon vagotomy. Large rostral pontile lesions did not change apneusis in spontaneous breathing animals whereas, in paralyzed, ventilated cats, these lesions resulted in some decrease of T i. It is concluded that apneusis generation is not equa table simply with a summation of caudal pontile respiratory unit activities. Rather, activity inherent to intrapontile and/or pontomedullary feedback circuits is considered as a necessary requisite for apneusis development. Interaction of these circuits with an inspiratory off-switch mechanism is considered probable.
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