M J Murray1, E S Eichorn. 1. Marion duPont Scott Equine Medical Center, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Leesburg 20177, USA.
Abstract
OBJECTIVES: To determine the effect of decreasing gastric acidity in a feed-deprivation protocol on induction of gastric ulcers, and to determine whether stall confinement may be a factor contributing to gastric ulceration in horses. ANIMALS: 8 adult horses, 4 geldings and 4 mares, 3 to 8 years old, and 7 adult horses, 5 geldings and 2 mares, 4 to 11 years old. PROCEDURE: Gastric ulceration was induced in horses by alternating 24-hour periods of feed deprivation and ad libitum access to hay, for a total of 96 hours' feed deprivation. This protocol was repeated with the horses receiving the histamine type-2 receptor (H2) antagonist ranitidine (6.6 mg/kg of body weight, PO, q 8 h). In another group of horses, severity of gastric lesions was compared after 7 days' pasture turnout and 7 days' stall confinement with ad libitum access to hay. Gastroscopy was performed after each feed-deprivation protocol was completed, and total lesion area in the gastric squamous epithelial mucosa was measured. Gastroscopy was performed at the beginning and end of 7 days' pasture turnout and 7 days' stall confinement. RESULTS: Alternating periods of feed deprivation resulted in erosion and ulceration of the gastric squamous epithelial mucosa of each horse. Concurrent treatment with ranitidine resulted in significantly (P < 0.05) less area of ulceration in the gastric squamous epithelial mucosa. After 7 days' stall confinement, 6 of 7 horses had ulceration in the gastric squamous epithelial mucosa, and 1 horse had a lesion in the glandular mucosa, whereas after 7 days' pasture turnout, 2 horses had reddening of the gastric squamous mucosa along the lesser curvature (P < 0.05). CONCLUSIONS AND CLINICAL RELEVANCE: Severe ulceration of the gastric squamous epithelial mucosa, caused by excess acidity, can develop rapidly in horses deprived of feed or not consuming feed. Suppression of gastric acidity with the histamine type-2 receptor antagonist ranitidine effectively minimized the area of ulceration caused by feed deprivation. Compared with being turned out to pasture, stall confinement alone appears to be an important factor in the development of gastric ulcers in horses, probably as a result of altered eating behavior.
OBJECTIVES: To determine the effect of decreasing gastric acidity in a feed-deprivation protocol on induction of gastric ulcers, and to determine whether stall confinement may be a factor contributing to gastric ulceration in horses. ANIMALS: 8 adult horses, 4 geldings and 4 mares, 3 to 8 years old, and 7 adult horses, 5 geldings and 2 mares, 4 to 11 years old. PROCEDURE: Gastric ulceration was induced in horses by alternating 24-hour periods of feed deprivation and ad libitum access to hay, for a total of 96 hours' feed deprivation. This protocol was repeated with the horses receiving the histamine type-2 receptor (H2) antagonist ranitidine (6.6 mg/kg of body weight, PO, q 8 h). In another group of horses, severity of gastric lesions was compared after 7 days' pasture turnout and 7 days' stall confinement with ad libitum access to hay. Gastroscopy was performed after each feed-deprivation protocol was completed, and total lesion area in the gastric squamous epithelial mucosa was measured. Gastroscopy was performed at the beginning and end of 7 days' pasture turnout and 7 days' stall confinement. RESULTS: Alternating periods of feed deprivation resulted in erosion and ulceration of the gastric squamous epithelial mucosa of each horse. Concurrent treatment with ranitidine resulted in significantly (P < 0.05) less area of ulceration in the gastric squamous epithelial mucosa. After 7 days' stall confinement, 6 of 7 horses had ulceration in the gastric squamous epithelial mucosa, and 1 horse had a lesion in the glandular mucosa, whereas after 7 days' pasture turnout, 2 horses had reddening of the gastric squamous mucosa along the lesser curvature (P < 0.05). CONCLUSIONS AND CLINICAL RELEVANCE: Severe ulceration of the gastric squamous epithelial mucosa, caused by excess acidity, can develop rapidly in horses deprived of feed or not consuming feed. Suppression of gastric acidity with the histamine type-2 receptor antagonist ranitidine effectively minimized the area of ulceration caused by feed deprivation. Compared with being turned out to pasture, stall confinement alone appears to be an important factor in the development of gastric ulcers in horses, probably as a result of altered eating behavior.
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