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. Intracerebroventricular pressure was maintained at 3, 8, or 13 cmH2O using normal saline perfused into the lateral cerebral ventricle and gastric antral and duodenal contractility was monitored using chronically implanted strain gauge force transducers. Gastric acid secretion was measured in a separate group of rabbits with chronically implanted gastric cannulas. Increased intracerebroventricular pressure (13 cmH2O) resulted in an immediate suppression of the amplitude of gastric and duodenal contractions by greater than 80% and greater than 60%, respectively. After normalization of intracerebroventricular pressure, the contractile pattern returned to basal levels. Intravenous bolus injection of bethanechol reversed the suppression of gastric antral contractility induced by increased intracranial pressure. Increased pressure for 2 h did not modify gastric acid output as compared with normal pressure controls, whereas atropine significantly inhibited and histamine stimulated gastric acid secretion in the same animals maintained at normal pressure. These results demonstrate that acutely increased intracranial pressure rapidly and reversibly inhibits gastric and duodenal motor function in conscious rabbits.

Cimetidine and ranitidine protect against cold restraint-induced ulceration in rat by suppressing gastric acid secretion.

The effect of the H2-receptor antagonists cimetidine and ranitidine on pentagastrin-stimulated gastric acid secretion in anesthetized rats, and gastric mucosal lesion formation and gastric motility in unanesthetized cold-restrained rats was studied. Both cimetidine and ranitidine suppressed pentagastrin-stimulated gastric secretion in a dose-dependent fashion. Cold restraint-induced lesion formation was not prevented with doses of both agents that inhibited acid secretion by 75%. Doses which suppressed pentagastrin-stimulated acid secretion more than 90% significantly prevented the development of gastric mucosal lesions produced by cold restraint. Doses of both H2 blockers which demonstrated significant suppression of lesion formation had no effect on cold restraint-stimulated gastric contractility. We conclude that cimetidine and ranitidine suppress cold restraint-induced lesion formation by suppressing acid secretion and not by suppressing gastric contractility.

Thyrotropin-releasing hormone (TRH) acts centrally to stimulate gastric contractility in rats.

Changes in gastric contractility induced by intracisternal (ic) injection of thyrotropin-releasing hormone (TRH) or a stable TRH analog, RX77368 [p-Glu-His-(3,3'-dimethyl)-Pro NH2] were investigated in 24 h fasted-conscious rats. Gastric contractility was monitored using chronically implanted extraluminal force transducers sutured to the corpus. Response elicited by a standard meal was used as a physiologic standard. Intracisternal injection of TRH (1 microgram) or RX77368 (100 ng), unlike saline, stimulated high amplitude gastric contractions. The stimulation of gastric contractions induced by ic RX77368 was dose dependent (3-100 ng), rapid in onset, long lasting and not mimicked by the intravenous route of administration. Atropine (0.1 mg/kg) partially antagonized and vagotomy totally blocked the RX77368 (100 ng, ic)-induced stimulation of gastric contractility. These results demonstrated that TRH or RX77368 acts within the brain to elicit potent contractions of the stomach; TRH action appears vagally mediated probably through cholinergic mechanism.

Gastric motility is stimulated but overall blood flow is unaffected during cold restraint in the rat.

The relationship between cold restraint-induced lesion formation, gastric motility, and gastric mucosal blood flow was studied in rats. Both anesthetized and unanesthetized animals placed in cold restraint developed gastric mucosal lesions. Gastric (corpus) motility was measured using extraluminal force transducers. Animals placed in cold restraint developed persistent, high amplitude, prolonged duration contractions. Those rats in which such contractions lasted greater than 1 h developed gastric mucosal lesions, whereas those animals in which such contractions lasted less than or equal to 1 h had no lesions. Overall gastric mucosal blood flow was measured using the hydrogen gas clearance technique. There was no significant change in overall gastric mucosal blood flow measured after 1, 2, and 3 h of cold restraint. We conclude that (a) the physical effect of cold water immersion is by itself sufficient to cause cold "restraint" lesions and (b) such lesions are associated with high amplitude, prolonged duration contractions lasting greater than 1 h.

Gastric motility is a major factor in cold restraint-induced lesion formation in rats.

These studies were performed to characterize the pattern of gastric contractility associated with cold restraint-induced lesion formation. Gastric motility in the rat was examined with extraluminal transducers at three sites of the stomach. The motility was monitored in the 24-h-fasted state, the postprandial state, and during cold-water immersion restraint. Gastric acid secretion was also monitored in a separate group of animals placed in cold restraint. Both feeding and cold restraint resulted in an equivalent increase in the amplitude of gastric contractions. Prolonged cold restraint, however, resulted in a distinct contractile pattern in which contractions were 56% less frequent and 300-400% longer in duration than those stimulated by feeding. All cold-restrained animals developed multiple gastric erosions. Cold restraint was not associated with increased acid secretion. A single subcutaneous injection of papaverine HCl (50 or 100 mg/kg) suppressed cold restraint-induced high-amplitude contractions and the cold restraint-induced lesion formation without altering acid secretion. These studies suggest that the stimulation of high-amplitude, prolonged duration contractions are more important than changes in gastric acid secretion in the formation of cold restraint-induced gastric lesions.