Murray M J, Eichorn E S
Marion duPont Scott Equine Medical Center, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Leesburg 20177, USA.
Am J Vet Res. 1996 Nov;57(11):1599-603.
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.
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.
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.
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).
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.
确定在禁食方案中降低胃酸对胃溃疡诱导的影响,并确定厩舍圈养是否可能是导致马胃溃疡的一个因素。
8匹成年马,4匹阉马和4匹母马,3至8岁;以及7匹成年马,5匹阉马和2匹母马,4至11岁。
通过交替进行24小时禁食期和随意采食干草期,共禁食96小时,诱导马发生胃溃疡。对接受组胺2型受体(H2)拮抗剂雷尼替丁(6.6mg/kg体重,口服,每8小时一次)的马重复该方案。在另一组马中,比较了在7天放牧和7天厩舍圈养(随意采食干草)后胃损伤的严重程度。在每个禁食方案完成后进行胃镜检查,并测量胃鳞状上皮粘膜的总损伤面积。在7天放牧和7天厩舍圈养的开始和结束时进行胃镜检查。
禁食期交替导致每匹马的胃鳞状上皮粘膜出现糜烂和溃疡。同时使用雷尼替丁治疗导致胃鳞状上皮粘膜溃疡面积显著减少(P<0.05)。在7天厩舍圈养后,7匹马中有6匹胃鳞状上皮粘膜出现溃疡,1匹马的腺性粘膜有损伤,而在7天放牧后,2匹马胃小弯侧的鳞状粘膜发红(P<0.05)。
在未进食或不采食饲料的马中,胃酸过多可导致胃鳞状上皮粘膜迅速发生严重溃疡。使用组胺2型受体拮抗剂雷尼替丁抑制胃酸,可有效减少禁食引起的溃疡面积。与放牧相比,仅厩舍圈养似乎是马发生胃溃疡的一个重要因素,可能是由于采食行为改变所致。