Respiratory frequency control during hypercapnia in vagotomized, anesthetized cats.

There is a small, but significant, increase in frequency during hypercapnia in vagotomized, anesthetized animals, indicating involvement of an extravagal mechanism in the response. The intent of this study was to determine the source of this second mechanism regulating frequency during hypercapnia. Experiments were performed on 22 vagotomized, anesthetized (Dial) cats. Frequency (f), inspiratory time (ti) and expiratory time (te) responses to CO2 were monitored before and after sectioning of afferent nerves from the carotid bodies (carotid sinus nerve section), chest wall (dorsal rhizotomies, T1-T12) and diaphragm (dorsal rhizotomies. C4-C7). Most vagotomized animals responded to 6% CO2 with an increased frequency, decreased ti and no consistent change in te. The responses to CO2 were essentially unaltered following chest wall and diaphragm deafferentation. Sodium cyanide stimulation of the carotid bodies produced similar respiratory pattern changes as CO2; furthermore, the f and ti changes with CO2 were still present following carotid body deafferentiation. The results of this study suggest that: (1) afferents from chest wall and diaphragm mechanoreceptors are not responsible for the vagal-like effects on ti and f during hypercapnia, (2) afferents from lung mechanoreceptors, via the vagus nerves, are the only inputs from respiratory mechanoreceptors causing an increased f during hypercapnia, (3) the extravagal mechanism responsible for the decreased ti and increased f during hypercapnia is inherent to the medullary-pontine rhythm generator, and (4) input from the chemoreceptors can elicit the response.