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Stress induced experimental colitis

机译:应激性实验性结肠炎

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摘要

Stress induces chemical changes in the central nervous system which alters the biochemistry and physiology of the digestive tract. The present study determines arachidonic acid oxidation and damage in the colon following stress. Ten rats were stressed by the cold-restraint method; ten were controls. Stress induced 0.5 ± 0.7 (S.D.) mucosal erosions whereas controls had none. Subepithelial hemorrhage and erosions occurred only in the proximal two-thirds of the colon. Prostaglandin E2 synthesis was increased after stress compared to the control (381 ± 130 vs. 1610 ± 372 ng/g/min). Leukotriene C4 synthesis also increased after stress (4217 ± 994 vs. 11300 ± 1662 ng/g/min). Synthesis of prostaglandin E2 increased (r = 0.9381) with leukotriene C4. The response of the colon to stress is less severe than that in the stomach and may be related to regional regulation of prostaglandin and leukotriene synthesis.
机译:压力会诱发中枢神经系统的化学变化,从而改变消化道的生物化学和生理学。本研究确定了花生四烯酸在应激后的氧化和结肠损伤。冷约束法对十只大鼠施加压力。十个是对照。压力引起0.5±0.7(S.D.)黏膜侵蚀,而对照组则没有。上皮下出血和糜烂仅发生在结肠的近三分之二处。与对照组相比,应激后前列腺素E2的合成增加(381±130与1610±372 ng / g / min)。应激后白三烯C4的合成也增加了(4217±994对11300±1662 ng / g / min)。白三烯C4使前列腺素E2的合成增加(r = 0.9381)。结肠对应激的反应不如在胃中严重,并且可能与前列腺素和白三烯合成的区域调节有关。

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