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首页> 外文期刊>Life sciences >Experimental colitis decreases rat jejunal amino acid absorption: role of capsaicin sensitive primary afferents.
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Experimental colitis decreases rat jejunal amino acid absorption: role of capsaicin sensitive primary afferents.

机译：实验性结肠炎会降低大鼠空肠氨基酸吸收：对辣椒素敏感的初级传入者的作用。

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Ulcerative colitis and experimental colitis are known to be associated with functional and structural abnormalities of the small intestine. The aim of this study was to determine whether experimental colitis in the rat has any effect on jejunal amino acid absorption and to investigate the neural mechanisms involved. In Sprague Dawley rats, colitis was induced by intracolonic administration of 0.1 ml of 6% iodoacetamide. Alanine absorption in the jejunum was measured using the single pass intraluminal perfusion technique in vivo and the three-compartment model in vitro. Experiments were done in normal and sham treated rats, as well as in rats that underwent neonatal capsaicin treatment, adult capsaicin treatment, or subdiaphragmatic vagotomy. Colitis was more severe in rats subjected to neonatal or adult capsaicin treatment, but was not affected by subdiaphragmatic vagotomy. In rats with colitis, jejunal alanine absorption was reduced by 2% (P>0.05), 28%, 40%, and 18% (P<0.001) at 1, 1.5, 2, and 3 days post rectal iodoacetamide administration. A rebound increase of 12% above baseline was noted at 4 days (P<0.05). Similar results were noted in vitro. In rats that received two consecutive injections of iodoacetamide, the decrease in jejunal alanine absorption occurred earlier, was more severe, and persisted for more than 30 days. Neonatal as well as adult capsaicin treatment aggravated both the colitis and the decrease in jejunal alanine absorption. On the other hand, subdiaphragmatic vagotomy attenuated the decrease in jejunal alanine absorption, but had no significant effect on colitis severity. It is concluded that iodoacetamide induced colitis impairs jejunal amino acid absorption and that this effect involves vagal efferents as well as capsaicin sensitive primary afferents.
机译：已知溃疡性结肠炎和实验性结肠炎与小肠的功能和结构异常有关。这项研究的目的是确定大鼠实验性结肠炎是否对空肠氨基酸吸收有任何影响，并研究所涉及的神经机制。在Sprague Dawley大鼠中，结肠内给药0.1 ml 6％的碘乙酰胺可诱发结肠炎。使用单次腔内灌注技术在体内和三室模型体外测量空肠中丙氨酸的吸收。实验在正常和假治疗的大鼠以及接受了新生辣椒素治疗，成年辣椒素治疗或dia肌下迷走神经切断术的大鼠中进行。在接受新生或成年辣椒素治疗的大鼠中，结肠炎更为严重，但不受dia下迷走神经切断术的影响。在患有结肠炎的大鼠中，直肠给药碘乙酰胺后1、1.5、2和3天，空肠丙氨酸吸收减少2％（P> 0.05），28％，40％和18％（P <0.001）。在第4天，反弹高于基线12％（P <0.05）。体外观察到相似的结果。在连续两次注射碘乙酰胺的大鼠中，空肠丙氨酸吸收的减少较早发生，更为严重，并持续超过30天。新生儿和成人辣椒素治疗均加重了结肠炎和空肠丙氨酸吸收的减少。另一方面，dia肌下迷走神经切断术减弱了空肠丙氨酸吸收的减少，但对结肠炎的严重程度没有显着影响。结论是碘乙酰胺诱发的结肠炎损害了空肠氨基酸吸收，并且这种作用涉及迷走神经传出以及对辣椒素敏感的初级传出。

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