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- Author or Editor: Jenifer A. Nadeau x
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Abstract
Objective
To measure total body water (TBW) content in horses, using deuterium oxide (D20) dilution.
Animals
Six 8- to 10-year-old healthy untrained mixed-breed horses, weighing (mean ± SD) 503.4 ± 64.0 kg.
Procedure
After a 12-hour nonfeeding period, 6 horses were given D2O (0.14 g/kg of body weight) via nasogastric tube. Blood samples were collected from a preplaced indwelling jugular vein catheter prior to and 1 to 8, 10, 12, 14, and 24 hours after administration of D2O. Blood samples were centrifuged immediately, and plasma was collected and stored at −70 C until analysis. The D2O content in plasma was measured by zinc reduction to deuterium gas. The resulting gas was measured, using an isotope ratio mass spectrometer.
Results
Deuterium oxide was rapidly absorbed from the gastrointestinal tract of all horses, and reached peak (mean ± SD) plasma concentration (1,454.4 ± 163 delta D/ml or parts/thousand) 1 hour after administration. Plasma concentration decreased slowly during the next 2 to 3 hours, then remained statistically constant from 2 to 5 hours (early plateau phase) and 3 to 7 hours (late plateau phase) after administration. Mean ± SEM TBW content was 623.0 ± 2.2 ml/kg (62.3% of body weight) for the early plateau phase and 630.3 ± 2.2 ml/kg (63.0% of body weight) for the late plateau phase.
Conclusion
Deuterium oxide dilution appears to be of value for measurement of TBW content in horses, and has a 4-hour plateau effect. Equilibration of D2O with large intestinal water may be the reason for the prolonged equilibrium time and plateau effect seen in these horses.
Clinical Relevance
Deuterium oxide appears safe and efficacious for determining TBW content in horses and may be helpful for determining changes in TBW content during exercise and disease. (Am J Vet Res 1997;58:1060–1064)
Abstract
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)
Abstract
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)
Abstract
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)
Abstract
Objectives
To determine the effects of orally administered omeprazole, as enteric-coated capsules, on baseline and stimulated gastric acid secretion in horses.
Animals
5 healthy 8-year-old mixed-breed horses fitted with gastric cannulas.
Procedure
Enteric-coated granules of omeprazole were mixed with corn syrup and administered orally once daily for 5 consecutive days. On days 1 and 5 beginning 5 hours after omeprazole administration, 4 gastric fluid samples were collected, each for 15 minutes, via the gastric cannula (baseline samples). Pentagastrin was administered IV as a constant infusion for the subsequent 2 hours, and 15-minute gastric fluid samples were again collected (stimulated samples). Fluid volume, acidity (mmol H+/L), and pH and gastric acid production (mmol H+) were determined for all baseline samples and for stimulated samples collected during the second hour of pentagastrin infusion. Control experiments were done in a similar manner after giving corn syrup alone to the same horses.
Results
Compared with values obtained during control experiments, baseline and stimulated gastric fluid acidity and gastric acid production significantly decreased, and the mean pH of gastric fluid samples significantly increased, after horses were given 5 daily doses of omeprazole.
Conclusions and Clinical Relevance
Enteric-coated omeprazole (1.0 mg/kg of body weight; PO) administered once daily for 5 days significantly inhibited unstimulated and pentagastrin-stimulated gastric acid secretion in horses. This commercially available formulation of omeprazole may be efficacious in the treatment of gastroduodenal ulcers in horses. (Am J Vet Res 1999;60:929–931)
