Intracerebroventricular pressure inhibits gastric antral and duodenal contractility but not acid secretion in conscious rabbits.

Acute nausea characteristically accompanies head injury or increased intracranial pressure, or both. The etiology of this symptom is unclear. We studied the effect of increased intracranial pressure on gastric antral and duodenal contractility and gastric acid secretion in conscious rabbits.

Central nervous system action of calcitonin to alter experimental gastric ulcers in rats.

The central nervous system action of calcitonin to influence various experimental models of gastric ulcers and gastric function was studied in rats fasted for 24 h. Intracisternal injection of salmon calcitonin (5 micrograms) completely suppressed gastric ulcerations induced by exposure to cold restraint stress, intracisternal injection of a stable thyrotropin-releasing hormone analogue, or peroral administration of aspirin. By contrast, intracisternal calcitonin enhanced gastric lesions elicited by peroral administration of 40% ethanol or 0.

Central nervous system action of TRH to stimulate gastric function and ulceration.

Intracisternal or intracerebroventricular injection of TRH (0.1-10 micrograms) in rats stimulated the secretion of gastric acid and pepsin secretion, increased gastric mucosal blood flow and gastric contractility and emptying, induced gastric hemorrhagic lesions and aggravated experimental ulcers elicited by aspirin, serotonin or indomethacin. TRH action was dose-dependent, rapid in onset and central nervous system-mediated by activation of the parasympathetic outflow to the stomach and cholinergic receptors.

Central nervous system action of corticotropin-releasing factor to inhibit gastric emptying in rats.

The present study evaluates the central nervous system action of rat corticotropin-releasing factor (CRF) on gastric emptying of a liquid meal in conscious rats using the phenol red method. Intracisternal injection of CRF (63-210 pmol) dose-dependently inhibited gastric emptying of a liquid meal by 37-80%. Peptide action was rapid in onset, long acting, and not mimicked by intracisternal injection of growth hormone-releasing factor.

Central nervous system action of TRH to stimulate gastric emptying in rats.

The effects of intracisternal injection of TRH on gastric emptying of a liquid meal was investigated in 24 h fasted rats using the phenol red method. Intracisternal injection of TRH, RX 77368, or [N-Val2]-TRH, an analog devoid of TSH-releasing activity, 5 min prior to a meal, stimulated gastric emptying measured 20 min later. TRH action was dose dependent (1-100 ng), and rapid in onset.