Effect of pyloric blockade and infusion of histamine or pentagastrin on gastric secretion in horses.

OBJECTIVE: To determine the origin of the nonacid (nonparietal) component of gastric secretions in horses induced by pentagastrin infusion. ANIMALS: 6 horses. PROCEDURE: A Latin square design was used, involving 6 horses, 3 treatments, and 2 duodenal intubation conditions (catheter with balloon to obstruct pylorus [B] or without balloon allowing movement of contents between stomach and duodenum [NB]). Each horse had an indwelling gastric cannula and a catheter positioned in the duodenum. Gastric and duodenal contents were collected during 15-minute periods. Each experiment consisted of serial collection periods: baseline; infusion of pyrilamine maleate (1 mg/kg of body weight, IV); not treated; and IV infusion of saline (0.9% NaCl) solution alone, saline solution containing pentagastrin (6 microg/kg x h), or saline solution containing histamine (30 microg/kg x h). Volume of samples was recorded, and electrolyte concentrations were measured. RESULTS: Pentagastrin and histamine stimulated maximal acid output; however, during NB conditions, pentagastrin-induced concentration of hydrogen ions was significantly less than during histamine or pentagastrin infusions during B conditions. The large volume produced in response to pentagastrin during NB conditions was accompanied by increased sodium ion output that was greater than for pentagastrin during B conditions, but both values were significantly greater than values for histamine during B or NB conditions. CONCLUSIONS AND CLINICAL RELEVANCE: Nonparietal secretions collected during IV infusion of pentagastrin are duodenal in origin. Reflux of duodenal contents into the stomach of horses is enhanced by pentagastrin. Flow of duodenal contents into the stomach could have implications in the pathogenesis of ulcers in horses.

Histamine-induced gastric acid secretion in horses.

OBJECTIVE: To determine gastric secretory responses in horses treated with histamine and to determine the dose of histamine needed to elicit maximal gastric secretion. ANIMALS: 6 adult horses with an indwelling gastric cannula. PROCEDURE: Gastric contents were collected in 15-minute periods, and volume, pH, hydrogen ion concentration, hydrogen ion output, sodium concentration, and sodium output were determined. Values were determined without any treatment (baseline), after administration of pyrilamine maleate (1 mg/kg of body weight, i.v., given during a 15-minute period), and during 1-hour infusions of histamine at 3 rates (7.5, 15, and 30 microg/kg/h, i.v.). RESULTS: Volume and hydrogen ion concentration of gastric contents and hydrogen ion output were significantly increased, compared with baseline values, during histamine infusion. Mean hydrogen ion concentration and hydrogen ion output were significantly greater during infusion of histamine at a rate of 15 or 30 microg/kg/h than at a rate of 7.5 microg/kg/h. Sodium concentration was significantly decreased, compared with baseline value, during histamine infusion, but sodium output was unchanged. CONCLUSIONS: Histamine at doses of 15 and 30 microg/kg/h, i.v. stimulated maximal gastric secretion in horses. Histamine appeared to induce only parietal secretion. CLINICAL RELEVANCE: This study provides additional information related to equine gastric physiology, which may benefit further understanding of the pathogenesis of peptic ulcer disease.

Type-I diabetes mellitus in a bull.

Although metabolic disorders are a frequent concern in cattle, they are not commonly recognized in bulls. The combination of hyperglycemia, acetonemia, ketonuria, and glycosuria in a bull was highly suggestive of diabetes mellitus. This uncommon diagnosis was confirmed by results of intravenous glucose tolerance testing. Results of the test and serum insulin values were further able to classify the disease in this bull as type-I diabetes mellitus.