Mechanisms of reflexes induced by esophageal distension

We investigated the mechanisms of esophageal distension-induced reflexes in decerebrate cats. Slow air esophageal distension activated esophago-upper esophageal sphincter (UES) contractile reflex (EUCR) and secondary peristalsis (2P). Rapid air distension activated esophago-UES relaxation reflex (EURR), esophago-glottal closure reflex (EGCR), esophago-hyoid distraction reflex (EHDR), and esophago-esophagus contraction reflex (EECR). Longitudinal esophageal stretch did not activate these reflexes. Magnitude and timing of EUCR were related to 2P but not injected air volume. Cervical esophagus transection did not affect the threshold of any reflex. Bolus diversion prevented swallow-related esophageal peristalsis. Lidocaine or capsaicin esophageal perfusion, esophageal mucosal layer removal, or intravenous baclofen blocked or inhibited EURR, EGCR, EHDR, and EECR but not EUCR or 2P. Thoracic vagotomy blocked all reflexes. These six reflexes can be activated by esophageal distension, and they occur in two sets depending on inflation rate rather than volume. EUCR was independent of 2P, but 2P activated EUCR; therefore, EUCR may help prevent reflux during peristalsis. All esophageal peristalsis may be secondary to esophageal stimulation in the cat. EURR, EHDR, EGCR, and EECR may contribute to belching and are probably mediated by capsaicin-sensitive, rapidly adapting mucosal mechanoreceptors. GABA-B receptors also inhibit these reflexes. EUCR and 2P are probably mediated by slowly adapting muscular mechanoreceptors. All six reflexes are mediated by vagal afferent fibers.

Evidence of a functional role in lung inflation for the buccal pump in the agamid lizard, Uromastyx aegyptius microlepis

This study has demonstrated that the agamid desert lizard Uromastyx aegyptius microlepis ventilates its lungs both with a triphasic, thoracic aspiratory pump and by gulping air, using a buccal pump. These two mechanisms never occur simultaneously because bouts of buccal pumping are always initiated after the passive expiration that terminates a thoracic breath. Lung inflation arising from thoracic and buccal ventilation was confirmed by direct recording of volume changes using a whole-body plethysmograph. This observation was further confirmed by mechanical separation of the inflationary pressures associated with these two breathing mechanisms, enabling the effects of lung inflation on buccal breathing to be observed. This revealed that the buccal pump is influenced by a powerful Hering-Breuer-type reflex, further confirming its role in lung inflation. Bilateral thoracic vagotomy tended to increase the variance of the amplitude and duration of the breaths associated with the aspiration pump and abolished the effects of lung inflation on the buccal pump. Uromastyx has vagal afferents from pulmonary receptors that respond to changes in lung volume and appear not to be sensitive to CO(2). This study describes two lung-inflation mechanisms (an amphibian-like buccal pump and a mammalian-like aspiration pump) in a single extant amniote, both of which are subject to vagal feedback control.

Centrally mediated stimulation of jejunal water and electrolyte secretion by calcitonin in dogs

The effects of intracerebroventricular versus intravenous injection of salmon calcitonin (sCT) at a dose of 0.2 IU X kg-1 on jejunal fluxes of water, Na+, and K+ were investigated before and after vagotomy or an intravenous treatment with indomethacin (1 mg X kg-1) in dogs prepared with a jejunal Thiry-Vella loop. Intestinal transport in the Thiry-Vella loop and concomitant mean transit time were measured during an infusion (2 ml X min-1) of an isotonic electrolyte solution and phenol red bolus injections. Basal net water absorption was significantly (P less than 0.01) reduced by 51.7% from 2 to 3 h after intracerebroventricular administration of sCT, Na+ absorption was reduced by 62.6%, and net flux of K+ was reversed from absorption to secretion. A similar intravenous dose had no effect. Previous treatment with indomethacin or bilateral thoracic vagotomy did not reduce the water, Na+, and K+ secretory effects of centrally administered sCT, whereas indomethacin per se appeared to reduce water and electrolyte absorption. A significant (P less than or equal to 0.05) increase in mean transit time was observed after intracerebroventricular but not intravenous calcitonin (0.2 IU X kg-1), and this effect was abolished after vagotomy. These results suggest that calcitonin may be involved in the central control of intestinal secretion in dog, inasmuch as these effects were mediated by different structures from those affecting intestinal motility.

Effect of thoracic vagotomy and vagal stimulation on esophageal function.

The purpose of this study was to determine the effect of thoracic vagotomy and thoracic vagal stimulation upon esophageal peristalsis and lower esophageal sphincter (LES) function in the opossum. The thoracic portion of the vagus nerve was sectioned in the upper or lower thorax. Bilateral, but not unilateral, thoracic vagotomy above the level of the heart abolished peristalsis and LES relaxation in response to swallowing or cervical vagal electrical stimulation. Thoracic vagotomy at the level of the ventricle or below did not alter either peristalsis or LES relaxation during swallowing or cervical vagal stimulation. Secondary peristalsis and its associated LES relaxation was unaltered by thoracic vagotomy at any level. Electrical stimulation of the distal end of the upper thoracic vagus elicited both peristalsis and LES relaxation. Electrical stimulation of the distal end of the lower thoracic vagus elicited both peristalsis and LES relaxation. Electrical stimulation of the distal end of the lower thoracic vagus, as well as stimulation of the vagal branches to the terminal esophagus, gave only LES relaxation. These studies suggest that: a) the major extrinsic vagal innervation mediating primary peristalsis terminates in the upper portion of the esophagus, whereas the vagal innervation mediating LES relaxation responses are present throughout the length of the esophagus; and b) secondary peristalsis and its associated LES relaxation occurs independent of extrinsic vagal innervation.

Effect of vagotomy on electrical activity of the small intestine of the dog

The effect of bilateral thoracic vagotomy on the myoelectric activity of the small intestine was determined in conscious dogs. Animals were implanted with electrodes spaced 25 cm apart along the serosal surface of the small intestine, and a cannula was placed in the most dependent portion of the stomach. Recordings were made with dogs in the fasted and fed states. Two distinct patterns of myoelectric activity were recorded: one typical of the fasted state (the interdigestive myoelectric complex) and one typical of the fed state. After completion of the control recording periods, a truncal vagotomy was performed on each animal. Completeness of vagotomy was confirmed by lack of a gastric secretory response to insulin. Gastric stasis occurred after vagotomy; therefore, the animals' stomachs were emptied via the gastric cannula to obtain a fasted condition. Vagotomy had little to no effect on the fasted pattern of myoelectric activity. The fed pattern was significantly altered in two of the three animals. This alteration could be due to the effect of vagotomy on gastrin release. We conclude that nervous pathways within the vagus may exert some influence on intestinal myoelectric activity but that other neural-humoral pathways are probably involved.