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大鼠胃扩张引起的黏膜病变

Mucosal lesions due to gastric distension in the rat.

作者信息

Gati T, Guth P H

出版信息

Am J Dig Dis. 1977 Dec;22(12):1083-90. doi: 10.1007/BF01072862.

Abstract

The pathogenesis of acute gastric mucosal lesions produced by distension of the rat stomach was studied. One hour of distension with 0.1 N HCl, but not saline, produced lesions in the glandular stomach in all rats. Histologic studies revealed marked thinning of the mucosa plus thrombus formation in the ulcerated area. Gastric distension with 8 ml HCl (per 100 g body weight) produced severe lesions, 4 ml minimal lesions and 2 ml no lesions. Intragastric pressure in the 8-ml group remained above 110 mm H2O for the first 10 min. Distension with 8 ml acid/100 g body weight for just 10 min resulted in significant lesion formation. Acid distension did not cause generalized disruption of the gastric mucosal barrier to H+ back-diffusion. It appears that an intragastric pressure of over 110 mm H2O for 10 min damages the mucosa by pressure (with thinning) and ischemia (with thrombosis), resulting in decreased resistance to acid peptic digestion and consequent acute lesion formation.

摘要

对大鼠胃扩张所致急性胃黏膜病变的发病机制进行了研究。用0.1N盐酸而非生理盐水扩张1小时,可使所有大鼠的腺胃出现病变。组织学研究显示,溃疡区域黏膜明显变薄并伴有血栓形成。用8毫升盐酸(每100克体重)进行胃扩张会产生严重病变,4毫升产生轻微病变,2毫升则无病变。8毫升组在最初10分钟内胃内压保持在110毫米水柱以上。以8毫升酸/100克体重仅扩张10分钟就会导致明显的病变形成。酸扩张并未引起胃黏膜屏障对氢离子反向扩散的普遍破坏。似乎胃内压超过110毫米水柱持续10分钟会通过压力(导致变薄)和缺血(导致血栓形成)损害黏膜,从而降低对胃酸消化的抵抗力并导致急性病变形成。

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