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T Garrick

Publications and source records attributed to T Garrick.

42 records · Page 3Linked to original sources

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.

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Neurobiologic and psychobiologic mechanisms in gastric function and ulceration.

The initiation and termination of feeding behavior are not fully understood. The stomach has been implicated as one source of signals regulating food intake. The sight and smell of food are potent stimuli to gastric acid secretion and contraction. The mouth, upper gastrointestinal tract and liver contain receptors regulating food intake; afferent information passes into the brain stem and into the brain areas. Lateral hypothalamic lesions abolish feeding, raise the body temperature and basal gastric acid secretion and produce gastric erosions. Vagotomy and administering propantheline bromide abolish the increased acid secretion after such lesions; they also alter the mucosal barrier permitting diffusion of protons into mucosal cells. Several of the neuropeptides via the central nervous system stimulate or inhibit gastric acid secretion through modulation of the autonomic nervous system. Most animal models of gastric erosions are associated with a reduced body temperature. Unknown is whether or not this association is the result of increased levels of thyrotropin-releasing hormone-a potent stimulus to gastric acid secretion and erosion formation when injected intracisternally.

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