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 motil ity during central and arterial chemoreceptor excitation or inhibition was analyzed in urethane anesthetized, artificially ventilated rats. Systemic severe hypoxia at end-tidal O2 concentration (FET(O2)) 6% and systemic hypercapnia at end-tidal CO2 concentration (FET(CO2)) 6%, 8% and 10% applied for 1 min produced a significant depression in gastri c tone and motility. Hypocapnia at 3% FET(CO2) increased gastric tone and motility. Hypoxia co-activated both the sympathetic and the vagal efferent gastric nerve branches. Hypercapnia augmented only sympatheti c gastric efferent nerve activity but not vagal efferent nerve activit y. Hypocapnia slightly increased vagal nerve activity to the stomach. Bilateral denervation of the arterial chemoreceptors significantly att enuated the inhibitory gastric response to hypoxia. Similar attenuatio n of hypoxia-induced depression of gastric tone and motility was produ ced by bilateral gastric sympathectomy but not by vagotomy. In contras t, the inhibitory effect of severe hypercapnia and the facilitatory ef fect of hypocapnia upon gastric tone and motility were unaffected by a rterial chemoreceptor denervation, by severance of gastric sympathetic branches or by gastric vagal denervation. Hyperoxia at 90% FET(O2) ha d 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 chemore ceptor reflex, and that hypercapnia activates sympathetic gastric nerv e activity via central chemoreceptors. Hypocapnia activates efferent v agal gastric nerve activity. All chemical stimuli except that of hyper oxia have a significant local effect on the gastric tone and motility. Hypoxia-induced depression depends on the contribution of activated g astric sympathetic nerves via arterial chemoreceptors. Stimulatory eff ects of hypocapnia are mainly local, with no significant contribution of the arterial or central chemoreceptors. Results obtained by applyin g severe hypercapnia do not provide evidence that arterial and central chemoreceptors contribute significantly to inhibition of gastric tone and motility by stimulation of gastric sympathetic nerve activity.