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- Author or Editor: Robert A. Argenzio x
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Objective—To identify the pathogenesis of gastric ulcers by comparing injury to the nonglandular gastric mucosa of horses caused by hydrochloric acid (HCl) or volatile fatty acids (VFAs).
Sample Population—Gastric tissues from 30 horses.
Procedure—Nonglandular gastric mucosa was studied by use of Ussing chambers. Short-circuit current (Isc) and potential difference were measured and electrical resistance calculated for tissues after addition of HCl and VFAs to normal Ringer's solution (NRS). Tissues were examined histologically.
Results—Mucosa exposed to HCl in NRS (pH, 1.5) had a significant decrease in Isc, compared with Isc for mucosa exposed to NRS at pH 4.0 or 7.0. Also, exposure to 60mM acetic, propionic, and butyric acids (pH, 4.0 or 1.5) caused an immediate significant decrease in Isc. Recovery of sodium transport was detected only in samples exposed to acetic acid at pH 4.0. Recovery of sodium transport was not seen in other mucosal samples exposed to VFAs at pH ≤ 4.0.
Conclusions and Clinical Relevance—Acetic, butyric, and propionic acids and, to a lesser extent, HCl caused decreases in mucosal barrier function of the nonglandular portion of the equine stomach. Because of their lipid solubility at pH ≤ 4.0, undissociated VFAs penetrate cells in the nonglandular gastric mucosa, which causes acidification of cellular contents, inhibition of sodium transport, and cellular swelling. Results indicate that HCl alone or in combination with VFAs at gastric pH ≤ 4.0 may be important in the pathogenesis of gastric ulcers in the nonglandular portion of the stomach of horses. (Am J Vet Res 2003;64:404–412)
Objective—To identify in vitro effects of hydrochloric acid, valeric acid, and other volatile fatty acids (VFAs) on the pathogenesis of ulcers in the nonglandular portion of the equine stomach.
Sample Population—Gastric tissues from 13 adult horses.
Procedure—Nonglandular gastric mucosa was studied by use of Ussing chambers. Short-circuit current (Isc) and potential difference were measured and electrical resistance and conductance calculated after tissues were bathed in normal Ringer's solution (NRS) or NRS and hydrochloric, valeric, acetic, propionic, and butyric acids. Treated tissues were examined histologically.
Results—Incubation in 60mM valeric acid at pH ≤ 7.0 abruptly and irreversibly abolished Isc, which was followed by a slower decrease in resistance and an increase in conductance. Incubation in 60mM acetic, propionic, and butyric acids and, to a lesser extent, hydrochloric acid at pH ≤ 7.0 significantly decreased Isc, which was followed by an increase in resistance and a decrease in conductance.
Conclusions and Clinical Relevance—Incubation in valeric acid at pH ≤ 7.0 caused a dramatic decrease in mucosal barrier function in the nonglandular portion of the stomach. Changes in barrier function attributable to exposure to valeric acid were associated with histopathologic evidence of cellular swelling in all layers of the nonglandular mucosa. Because of its high lipid solubility, valeric acid penetrates the nonglandular gastric mucosa, resulting in inhibition of sodium transport and cellular swelling. Valeric acid and other VFAs in gastric contents may contribute to the pathogenesis of ulcers in the nonglandular portion of the stomach of horses. (Am J Vet Res 2003;64:413–417)
Objective—To measure pH, volatile fatty acid (VFA) concentrations, and lactate concentrations in stomach contents and determine number and severity of gastric lesions in horses fed bromegrass hay and alfalfa hay-grain diets.
Animals—Six 7-year-old horses.
Procedure—A gastric cannula was inserted in each horse. Horses were fed each diet, using a randomized crossover design. Stomach contents were collected immediately after feeding and 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, and 24 hours after feeding on day 14. The pH and VFA and lactate concentrations were measured in gastric juice. Number and severity of gastric lesions were scored during endoscopic examinations.
Results—The alfalfa hay-grain diet caused significantly higher pH in gastric juice during the first 5 hours after feeding, compared with that for bromegrass hay. Concentrations of acetic, propionic, and isovaleric acid were significantly higher in gastric juice, and number and severity of nonglandular squamous gastric lesions were significantly lower in horses fed alfalfa hay-grain. Valeric acid, butyric acid, and propionic acid concentrations and pH were useful in predicting severity of nonglandular squamous gastric lesions in horses fed alfalfa hay-grain, whereas valeric acid concentrations and butyric acid were useful in predicting severity of those lesions in horses fed bromegrass hay.
Conclusions and Clinical Relevance—An alfalfa haygrain diet induced significantly higher pH and VFA concentrations in gastric juice than did bromegrass hay. However, number and severity of nonglandular squamous gastric lesions were significantly lower in horses fed alfalfa hay-grain. An alfalfa hay-grain diet may buffer stomach acid in horses. (Am J Vet Res 2000;61: 784–790)
Objective—To develop an endoscopic technique for use in monitoring devlopment of gastric ulcers via a gastric cannula during withholding of feed and administration of a finely ground diet to pigs.
Animals—6 pigs weighing between 60 and 70 kg.
Procedure—A gastric cannula was surgically inserted adjacent to the pars esophagea in each pig. Pigs were fed a finely ground diet for two 7-day periods that were separated by a 48-hour period during which feed was withheld. Endoscopic examination via the gastric cannula was used to monitor development of ulcers in the pars esophageal region of the pigs during the 48-hour period of feed withhold and subsequent 7-day feeding period. An ulcer score was assigned during each endoscopic examination. A final examination was performed during necropsy and compared with results for the final endoscopic examination.
Results—Consumption of a finely ground diet for 7 days resulted in progressive erosive damage to the pars esophageal region of the stomach. Further significant increases in ulcerative damage were detected after 24 and 48 hours of withholding of feed. Final examination during necropsy did not reveal significant differences from results obtained during the final endoscopic examination.
Conclusions and Clinical Relevance—Endoscopic examination via a gastric cannula was an effective means of monitoring ulcer development in the pars esophagea of pigs. Feeding a finely ground diet and withholding of feed induced endoscopically observable ulcers in the stratified squamous epithelial region of the stomach. Direct visual examination during necropsy confirmed the accuracy of endoscopic examination. (Am J Vet Res 2002;63:1076–1082)
Objective—To evaluate intestinal permeability and gluten sensitivity in a family of Soft-Coated Wheaten Terriers (SCWT) affected with protein-losing enteropathy (PLE), protein-losing nephropathy (PLN), or both.
Animals—6 affected adult dogs.
Procedure—Intestinal biopsy specimens, urine protein- to-creatinine ratio, serum concentrations of albumin and globulin, and concentration of α1-protease inhibitor in feces were evaluated before, during, and 13 weeks after daily administration of 10 g of gluten for 7 weeks. Eosinophils and lymphocytes-plasmacytes were enumerated in intestinal biopsy specimens. Intestinal permeability was evaluated before and during the sixth week of gluten administration via cellobiose-mannitol and chromium-EDTA absorption tests.
Results—Serum globulin concentration decreased significantly after prolonged administration of gluten. Although not significant, there was an increase in lymphocytes- plasmacytes and a decrease in eosinophils in intestinal biopsy specimens. Furthermore, these counts were greater than those reported for clinically normal dogs. Gluten administration did not increase intestinal permeability.
Conclusions and Clinical Relevance—Daily administration of gluten was associated with a significant decrease in serum globulin concentration in SCWT affected with PLE or PLN, but other variables remained unchanged. Although enhanced wheatgluten sensitivity may be one factor involved in the pathogenesis of PLE or PLN in SCWT, this syndrome does not appear to be the result of a specific sensitivity to gluten. (Am J Vet Res 2000;61:518–524)