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在结肠溃疡的实验模型中,结肠肠系膜缘最易受到损伤。

The colonic mesenteric margin is most susceptible to injury in an experimental model of colonic ulceration.

作者信息

Anthony A, Dhillon A P, Pounder R E, Wakefield A J

机构信息

Inflammatory Bowel Disease Study Group, University Departments of Medicine and Histopathology, Royal Free and University College Medical School, London, UK.

出版信息

Aliment Pharmacol Ther. 1999 Apr;13(4):531-5. doi: 10.1046/j.1365-2036.1999.00495.x.

DOI:10.1046/j.1365-2036.1999.00495.x
PMID:10215739
Abstract

BACKGROUND

Crohn's disease ileal ulcers and indomethacin-induced jejunal ulceration in the rat tend to occur in the mucosa nearest to the mesentery (mesenteric margin), an area of the bowel wall that has a critical blood supply. Mercuric chloride induces caecal and colonic ulceration in the Brown Norway rat.

AIM

To examine whether the mesenteric margin is more sensitive to injury by a substance known to be vasculotoxic in the caecum and colon.

METHODS

Brown Norway rats received a single subcutaneous dose of either mercuric chloride 1 mg/kg or saline. The gastrointestinal tract was examined macro- and microscopically for lesions 48 h later. The vascular anatomy of the normal rat colon and caecum was also examined using the carbon ink perfusion technique.

RESULTS

Mercuric chloride induced caecal and colonic ulceration preferentially along the mesenteric margin of the bowel wall. Histologically, the lesions showed mucosal necrosis and neutrophil infiltration. There was also extensive vascular degeneration/necrosis with microaneurysm formation and extensive submucosal haemorrhage. Cellular infiltration of the vasculature was not a feature. The caecal and colonic mesenteric margins in control rats were supplied by small end arteries.

CONCLUSIONS

The colonic and caecal mesenteric margins are susceptible to injury by mercuric chloride, a chemical known to induce haemorrhagic vasculopathy in the rat gastrointestinal tract. The large bowel mesenteric margin may be susceptible to injury by mercuric chloride because of the critical blood supply to that side of the bowel wall.

摘要

背景

克罗恩病的回肠溃疡以及吲哚美辛诱导的大鼠空肠溃疡往往发生在最靠近肠系膜(系膜缘)的黏膜处,肠系膜缘是肠壁中血液供应至关重要的区域。氯化汞可诱导棕色挪威大鼠的盲肠和结肠溃疡形成。

目的

研究系膜缘对一种已知在盲肠和结肠具有血管毒性的物质所致损伤是否更为敏感。

方法

棕色挪威大鼠皮下单次注射1 mg/kg氯化汞或生理盐水。48小时后对胃肠道进行大体和显微镜检查以观察损伤情况。还采用碳墨灌注技术检查正常大鼠结肠和盲肠的血管解剖结构。

结果

氯化汞优先沿肠壁的系膜缘诱导盲肠和结肠溃疡形成。组织学上,病变表现为黏膜坏死和中性粒细胞浸润。还存在广泛的血管变性/坏死、微动脉瘤形成以及广泛的黏膜下出血。血管的细胞浸润并非其特征。对照大鼠的盲肠和结肠系膜缘由小终末动脉供血。

结论

结肠和盲肠的系膜缘易受氯化汞损伤,氯化汞是一种已知可在大鼠胃肠道诱导出血性血管病的化学物质。大肠系膜缘可能因肠壁该侧关键的血液供应而易受氯化汞损伤。

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The colonic mesenteric margin is most susceptible to injury in an experimental model of colonic ulceration.在结肠溃疡的实验模型中,结肠肠系膜缘最易受到损伤。
Aliment Pharmacol Ther. 1999 Apr;13(4):531-5. doi: 10.1046/j.1365-2036.1999.00495.x.
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Similarities between ileal Crohn's disease and indomethacin experimental jejunal ulcers in the rat.大鼠回肠克罗恩病与吲哚美辛所致实验性空肠溃疡的相似性
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