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肾衰竭大鼠水浸应激诱导胃溃疡的发病机制

Pathogenesis of water-immersion stress-induced gastric ulcers in rats with renal failure.

作者信息

Suzuki Y, Kameyama J, Nishina M, Tsukamoto M, Nishiyama N, Ishihara K, Hotta K

机构信息

Department of Surgery, Yamagata University School of Medicine, Japan.

出版信息

Scand J Gastroenterol Suppl. 1989;162:127-30. doi: 10.3109/00365528909091142.

Abstract

Rats with or without renal failure, produced by uranyl acetate, were subjected to water-immersion stress for 6 h. The severity of stress-induced gastric ulcers in the renal failure group was significantly higher than that in the control group. The intragastric pH did not significantly differ between the two groups. Transmucosal electrical potential difference, gastric mucosal blood flow, and gastric mucosal hexosamine content in the renal failure group were significantly lower than in the control group. These results suggest that decreases in defensive factors, rather than an increase in an aggressive factor, may be more closely involved in the development of acute gastric ulcers in rats with renal failure.

摘要

通过醋酸铀酰诱导产生或未产生肾衰竭的大鼠,接受6小时的水浸应激。肾衰竭组应激诱导的胃溃疡严重程度显著高于对照组。两组的胃内pH值无显著差异。肾衰竭组的跨黏膜电位差、胃黏膜血流量和胃黏膜己糖胺含量显著低于对照组。这些结果表明,防御因素的降低而非攻击因素的增加,可能与肾衰竭大鼠急性胃溃疡的发生更为密切相关。

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