Role of vagal fibers in the hypoxia-induced increases in end-expiratory lung volume and diaphragmatic activity.

Abstract

The possible role of pulmonary C fibers in the hypoxia-induced concomitant increases in end-expiratory lung volume (EELV) and in the activity of the diaphragm at the end of expiration (DE) were evaluated by measuring the effects of hypoxia (10% O2) on ventilation, EELV, and DE in eight chloralose-urethan anesthetized rats. Recordings were made before and after blocking vagal C fibers and after bilateral vagotomy. C-fiber conduction was blocked by applying capsaicin perineurally to the cervical vagi. The efficiency of C-fiber blockade was tested with intravenous capsaicin and its selectivity by the Hering-Breuer reflex. Perineural capsaicin abolished the reflex apnea induced by intravenous capsaicin and transiently reduced Hering-Breuer reflex. Perineural capsaicin affected neither ventilation, DE, and EELV in air nor the hypoxia-induced increases in these parameters. Vagotomy caused the typical changes of breathing pattern in air, but the ventilatory response to hypoxia was unchanged. Vagotomy performed during hypoxia resulted in large decreases in DE and EELV. Hypoxia increased DE and EELV in vagotomized rats but less than in intact rats. We conclude that the hypoxia-induced increases in EELV and diaphragmatic activity are probably not mediated by vagal C fibers and that vagal afferents are involved but not fully responsible for this phenomenon.