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大鼠远端结肠反复炎症后体外自发性收缩的改变

Alterations in spontaneous contractions in vitro after repeated inflammation of rat distal colon.

作者信息

Bossone C, Hosseini J M, Piñeiro-Carrero V, Shea-Donohue T

机构信息

Department of Physiology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, USA.

出版信息

Am J Physiol Gastrointest Liver Physiol. 2001 May;280(5):G949-57. doi: 10.1152/ajpgi.2001.280.5.G949.

DOI:10.1152/ajpgi.2001.280.5.G949
PMID:11292604
Abstract

In inflammatory bowel disease, smooth muscle function reportedly varies with disease duration. The aim of these studies was to determine changes in the control of spontaneous contractions in a model of experimental colitis that included reinflammation of the healed area. The amplitude and frequency of spontaneous contractions in circular smooth muscle were determined after intrarectal administration of trinitrobenzenesulfonic acid in rat distal colon. With the use of a novel paradigm, rats were studied 4 h (acute) or 28 days (healed) after the initial inflammation. At 28 days, rats were studied 4 h after a second inflammation (reinflamed) of the colon. Colitis induced transient increases in the amplitude of spontaneous contractions coincident with a loss of nitric oxide synthase activity. The frequency of contractions was controlled by constitutive nitric oxide in controls. Frequency was increased in healed and reinflamed colon and was associated with a shift in the dominance of neural constitutive nitric oxide synthase control to that of inducible nitric oxide synthase (iNOS). The initial colitis induced a remodeling of the neural control of spontaneous contractions reflecting changes in their regulation by constitutive nitric oxide synthase and iNOS.

摘要

在炎症性肠病中,据报道平滑肌功能会随疾病持续时间而变化。这些研究的目的是确定在一个包括愈合区域再次发炎的实验性结肠炎模型中,自发收缩控制的变化情况。在大鼠远端结肠内直肠给予三硝基苯磺酸后,测定环形平滑肌自发收缩的幅度和频率。采用一种新的模式,在初次炎症后4小时(急性)或28天(愈合)对大鼠进行研究。在28天时,对大鼠在结肠第二次发炎(再次发炎)后4小时进行研究。结肠炎导致自发收缩幅度短暂增加,同时一氧化氮合酶活性丧失。在对照组中,收缩频率由组成型一氧化氮控制。在愈合和再次发炎的结肠中,频率增加,并且与神经组成型一氧化氮合酶控制的优势向诱导型一氧化氮合酶(iNOS)的转变有关。最初的结肠炎诱导了自发收缩神经控制的重塑,反映了其受组成型一氧化氮合酶和iNOS调节的变化。

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