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在大鼠结肠炎模型中,炎症消退后内脏高敏感性和结肠动力改变。

Visceral hypersensitivity and altered colonic motility after subsidence of inflammation in a rat model of colitis.

作者信息

La Jun-Ho, Kim Tae-Wan, Sung Tae-Sik, Kang Jeoung-Woo, Kim Hyun-Ju, Yang Il-Suk

机构信息

Department of Physiology, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.

出版信息

World J Gastroenterol. 2003 Dec;9(12):2791-5. doi: 10.3748/wjg.v9.i12.2791.

DOI:10.3748/wjg.v9.i12.2791
PMID:14669335
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4612054/
Abstract

AIM

Irritable bowel syndrome (IBS) is a functional bowel disorder characterized by visceral hypersensitivity and altered bowel motility. There is increasing evidence suggesting the role of inflammation in the pathogenesis of IBS, which addresses the possibility that formerly established rat model of colitis could be used as an IBS model after the inflammation subsided.

METHODS

Colitis was induced by intracolonic instillation of 4% acetic acid in male Sprague-Dawley rats. The extent of inflammation was assessed by histological examination and myeloperoxidase (MPO) activity assay. After subsidence of colitis, the rats were subjected to rectal distension and restraint stress, then the abdominal withdrawal reflex and the number of stress-induced fecal output were measured, respectively.

RESULTS

At 2 days post-induction of colitis, the colon showed characteristic inflammatory changes in histology and 8-fold increase in MPO activity. At 7 days post-induction of colitis, the histological features and MPO activity returned to normal. The rats at 7 days post-induction of colitis showed hypersensitive response to rectal distension without an accompanying change in rectal compliance, and defecated more stools than control animals when under stress.

CONCLUSION

These results concur largely with the characteristic features of IBS, visceral hypersensitivity and altered defecation pattern in the absence of detectable disease, suggesting that this animal model is a methodologically convenient and useful model for studying a subset of IBS.

摘要

目的

肠易激综合征(IBS)是一种功能性肠病,其特征为内脏高敏感性和肠道运动改变。越来越多的证据表明炎症在IBS发病机制中起作用,这提示先前建立的大鼠结肠炎模型在炎症消退后可作为IBS模型。

方法

通过向雄性Sprague-Dawley大鼠结肠内注入4%乙酸诱导结肠炎。通过组织学检查和髓过氧化物酶(MPO)活性测定评估炎症程度。结肠炎消退后,对大鼠施加直肠扩张和束缚应激,然后分别测量腹部回撤反射和应激诱导的粪便排出量。

结果

在诱导结肠炎后2天,结肠在组织学上呈现特征性炎症变化,MPO活性增加8倍。在诱导结肠炎后7天,组织学特征和MPO活性恢复正常。诱导结肠炎后7天的大鼠对直肠扩张表现出高敏反应,直肠顺应性无伴随变化,且在应激状态下比对照动物排便更多。

结论

这些结果在很大程度上与IBS的特征相符,即在无可检测疾病的情况下出现内脏高敏感性和排便模式改变,表明该动物模型是研究IBS一个亚组的方法简便且有用的模型。

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