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The Autonomic Control of Colonic Mucin Secretion in the Mouse

机译:小鼠结肠粘蛋白分泌的自主控制

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摘要

The mucosal secretion of the mouse colon is partly sialomucin and partly sulphomucin. The former acts to protect the epithelium and the latter may act as a less viscid lubricant. The protective action of the former is so good that even full thickness trauma to the mucosa initiates no inflammatory response, presumably because it prevents the release of any pharmacologically active substances. Carbachol produces considerable epithelial shedding, resulting eventually in large mucosal deficiencies, but the mucin layer remains intact and there is no ulceration or inflammatory reaction. There is oversecretion of mucin but probably no effect on synthesis. Beta adrenergic stimulating drugs produce increased mucin synthesis and secretion, swelling of epithelial cells and inflammatory infiltration of the mucosa with retention of cellular debris and polymorphs in the crypts. Beta adrenergic blocking agents produce haemorrhage and inflammation acutely, which is probably due to ischaemia, and in the long-term shortening and thickening of the muscle coats.
机译:小鼠结肠的粘膜分泌部分是唾液白蛋白,部分是磺基粘蛋白。前者起保护上皮的作用,而后者起粘稠度较小的润滑剂的作用。前者的保护作用是如此之好,以至于粘膜的全层创伤都不会引发炎症反应,这大概是因为它阻止了任何药理活性物质的释放。卡巴胆碱产生大量的上皮脱落,最终导致大的粘膜缺陷,但粘蛋白层保持完整,没有溃疡或炎症反应。粘蛋白分泌过多,但可能对合成没有影响。 β肾上腺素能刺激药物可增加粘蛋白的合成和分泌,上皮细胞肿胀和粘膜发炎性浸润,并在隐窝中保留细胞碎片和多晶型物。 β肾上腺素能阻断剂会急性产生出血和炎症,这可能是由于缺血引起的,并且长期会导致皮层的缩短和增厚。

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