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肝前性门静脉高压会使大鼠小肠和肠系膜淋巴结中的肥大细胞密度增加。

Prehepatic portal hypertension produces increased mast cell density in the small bowel and in mesenteric lymph nodes in the rat.

作者信息

Prieto Isabel, Aller María-Angeles, Santamaría Luis, Nava María-Paz, Madero Rosario, Pérez-Robledo Juan-Pedro, Arias Jaime

机构信息

Surgery I Department, School of Medicine, Complutense University of Madrid, Madrid, Spain.

出版信息

J Gastroenterol Hepatol. 2005 Jul;20(7):1025-31. doi: 10.1111/j.1440-1746.2005.03831.x.

DOI:10.1111/j.1440-1746.2005.03831.x
PMID:15955210
Abstract

BACKGROUND

Because most of the characteristics of the portal hypertensive enteropathy can be explained on the basis of increased levels of mast cell mediators, the purpose of the present paper was to study mast cell splanchnic infiltration.

METHODS

Duodenum, jejunum, ileum and mesenteric lymph node complex infiltration by mast cells was assayed by a stereological technique in control rats (group I; n = 5) and in an experimental model of portal hypertension (the portal vein-stenosed rat, group II; n = 5) at 6 weeks after operation.

RESULTS

Intestinal and mesenteric lymph node complex infiltration by mast cells increased in the animals with partial portal vein ligation. The mast cell density progressively increased distally along the small bowel. The mast cell increase in the mesenteric lymph node complex in portal vein-stenosed rats was greater than in the duodenum (P = 0.001), jejunum (P = 0.006) and ileum.

CONCLUSION

The rise of mast cells density in the small bowel and mesenteric lymph node complex in rats with partial portal vein ligation suggests that these cells are involved in the etiopathogenesis of experimental portal prehepatic hypertensive enteropathy.

摘要

背景

由于门脉高压性肠病的大多数特征可基于肥大细胞介质水平升高来解释,因此本文旨在研究肥大细胞在内脏的浸润情况。

方法

采用体视学技术,对对照组大鼠(I组;n = 5)和门脉高压实验模型(门静脉狭窄大鼠,II组;n = 5)术后6周的十二指肠、空肠、回肠及肠系膜淋巴结复合体中肥大细胞的浸润情况进行测定。

结果

部分门静脉结扎的动物中,肠道及肠系膜淋巴结复合体中肥大细胞的浸润增加。肥大细胞密度沿小肠向远端逐渐增加。门静脉狭窄大鼠肠系膜淋巴结复合体中肥大细胞的增加幅度大于十二指肠(P = 0.001)、空肠(P = 0.006)和回肠。

结论

部分门静脉结扎大鼠小肠及肠系膜淋巴结复合体中肥大细胞密度的升高表明,这些细胞参与了实验性肝前门脉高压性肠病的发病机制。

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