Role of the central and arterial chemoreceptors in the response of gastric tone and motility to hypoxia, hypercapnia and hypocapnia in rats.

The contribution of autonomic nerve activity to stomach tone and motility during central and arterial chemoreceptor excitation or inhibition was analyzed in urethane anesthetized, artificially ventilated rats. Systemic severe hypoxia at end-tidal O2 concentration (FETO2) 6% and systemic hypercapnia at end-tidal CO2 concentration (FETCO2) 6%, 8% and 10% applied for 1 min produced a significant depression in gastric tone and motility. Hypocapnia at 3% FETCO2 increased gastric tone and motility. Hypoxia co-activated both the sympathetic and the vagal efferent gastric nerve branches. Hypercapnia augmented only sympathetic gastric efferent nerve activity but not vagal efferent nerve activity. Hypocapnia slightly increased vagal nerve activity to the stomach. Bilateral denervation of the arterial chemoreceptors significantly attenuated the inhibitory gastric response to hypoxia. Similar attenuation of hypoxia-induced depression of gastric tone and motility was produced by bilateral gastric sympathectomy but not by vagotomy. In contrast, the inhibitory effect of severe hypercapnia and the facilitatory effect of hypocapnia upon gastric tone and motility were unaffected by arterial chemoreceptor denervation, by severance of gastric sympathetic branches or by gastric vagal denervation. Hyperoxia at 90% FETO2 had no effect on the gastric nerve activities, gastric tone or motility. It is concluded that in the rat hypoxia co-activates sympathetic and vagal efferent nerve activities to the stomach via an arterial chemoreceptor reflex, and that hypercapnia activates sympathetic gastric nerve activity via central chemoreceptors. Hypocapnia activates efferent vagal gastric nerve activity. All chemical stimuli except that of hyperoxia have a significant local effect on the gastric tone and motility.(ABSTRACT TRUNCATED AT 250 WORDS)