Intravenous glucose infusion decreases intracisternal thyrotropin-releasing hormone induced vagal stimulation of gastric acid secretion in anesthetized rats.

Gastroparesis is a common complication of diabetes attributed to autonomic neuropathy. This study investigated whether acute hyperglycemia influences central thyrotropin-releasing hormone (TRH), a well-established brain medullary vagal stimulus, induced gastric acid secretion in overnight fasted, urethane-anesthetized rats. Intravenous infusion of D-glucose (20%, 30% and 40%) dose dependently reduced intracisternal TRH-induced gastric acid secretion (71+/-28 micromol/90 min) by 39%, 90% and 100% respectively. Pretreatment with cholecystokinin(A) (CCK(A)) receptor antagonist devazepide (1 mg/kg) did not influence the inhibitory effect of intravenous glucose (30%). These results indicate that hyperglycemia may have a central effect to antagonize medullary TRH stimulation of vagal outflow to the stomach.