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急性胃黏膜病变——一种新的实验模型及肠外营养的作用

Acute gastric mucosal lesions--a new experimental model and effect of parenteral nutrition.

作者信息

Nakagawa K, Okada A, Kawashima Y

出版信息

JPEN J Parenter Enteral Nutr. 1985 Sep-Oct;9(5):571-82. doi: 10.1177/0148607185009005571.

DOI:10.1177/0148607185009005571
PMID:3930764
Abstract

Experiments were performed on 94 male Sprague-Dawley rats to explore the influence of starvation and parenteral nutrition on the development of acute gastric mucosal changes under stress. Comparative assessments were made of lesions in the gastric mucosa of rats on 1- or 6-day repeated exposure to the stress consisting of restraint with immersion in water. Marked hemorrhagic lesions over the extensive area of the glandular stomach and pronounced ulcerative changes in the nonglandular stomach were observed in 6-day stress group as compared to 1-day stress group where only a few hemorrhagic lesions were observed. Thus, this model has proven to provide an excellent experimental model suitable to the purpose of the present investigation. Parenteral nutrition significantly suppressed the development of mucosal damage either in the nonglandular or glandular stomach of rats under 6-day stress. Furthermore, it has been demonstrated that lesions caused in the glandular stomach increase in severity via exposure to stress and starvation while those evoked in the nonglandular stomach rise in incidence even in the presence of starvation alone.

摘要

对94只雄性Sprague-Dawley大鼠进行实验,以探究饥饿和肠外营养对应激状态下急性胃黏膜变化发展的影响。对大鼠胃黏膜病变进行了比较评估,这些大鼠1天或6天反复暴露于由束缚并浸入水中构成的应激状态。与仅观察到少数出血性病变的1天应激组相比,6天应激组在腺胃大面积出现明显的出血性病变,非腺胃出现明显的溃疡性变化。因此,该模型已被证明是适合本研究目的的优秀实验模型。肠外营养显著抑制了6天应激状态下大鼠非腺胃或腺胃黏膜损伤的发展。此外,已经证明,腺胃中由应激和饥饿引起的病变严重程度会增加,而即使仅存在饥饿,非腺胃中诱发的病变发生率也会上升。

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Eur J Clin Microbiol Infect Dis. 1989 Jan;8(1):51-5. doi: 10.1007/BF01964120.