Collins S M, McHugh K, Jacobson K, Khan I, Riddell R, Murase K, Weingarten H P
Intestinal Diseases Research Unit, McMaster University, Hamilton, Ontario, Canada.
Gastroenterology. 1996 Dec;111(6):1509-15. doi: 10.1016/s0016-5085(96)70012-4.
BACKGROUND & AIMS: Patients with inflammatory bowel disease have symptoms of irritable bowel syndrome (IBS) with a higher than expected prevalence. Stress is an important factor in the pathogenesis of IBS. Thus, previous inflammation may predispose to IBS by rendering the bowel more susceptible to the impact of stress. The aim of this study was to examine the effect of previous colitis on stress-induced responses in rats.
Acute colitis was induced in rats by intrarectal administration of trinitrobenzene sulfonic acid (TNBS), and the rats were allowed to recover for 6 weeks before application of mild restraint stress for 3 consecutive days. In vitro measurements included myeloperoxidase activity, plasma corticosterone levels, interleukin 1 beta messenger RNA expression, and [3H]noradrenaline release from the myenteric plexus.
Six weeks after administration of TNBS, stress caused a significant increase in myeloperoxidase activity in TNBS-treated rats but not in stressed controls; plasma corticosterone responses were similar. Stress also caused an exaggerated and significant suppression of [3H]noradrenaline release in TNBS-treated stressed rats compared with stressed controls. This was accompanied by a significant decrease in interleukin 1 beta messenger RNA expression in the colon.
Previous colitis rendered the colon more susceptible to effects of stress on enteric nerve function and also increased some parameters of inflammation in response to stress.
炎症性肠病患者出现肠易激综合征（IBS）症状的患病率高于预期。应激是IBS发病机制中的一个重要因素。因此，既往炎症可能通过使肠道对应激的影响更敏感而导致IBS。本研究的目的是探讨既往结肠炎对大鼠应激诱导反应的影响。
通过直肠内给予三硝基苯磺酸（TNBS）诱导大鼠急性结肠炎，让大鼠恢复6周后，连续3天施加轻度束缚应激。体外测量包括髓过氧化物酶活性、血浆皮质酮水平、白细胞介素1β信使核糖核酸表达以及肠肌间神经丛中[3H]去甲肾上腺素的释放。
给予TNBS 6周后，应激导致TNBS处理组大鼠的髓过氧化物酶活性显著增加，而应激对照组未增加；血浆皮质酮反应相似。与应激对照组相比，应激还导致TNBS处理的应激大鼠中[3H]去甲肾上腺素释放受到过度且显著的抑制。这伴随着结肠中白细胞介素1β信使核糖核酸表达的显著降低。
既往结肠炎使结肠对应激对肠神经功能的影响更敏感，并且在应激反应中也增加了一些炎症参数。
