TRANSMISSIBLE GASTROENTERITIS - MECHANISMS RESPONSIBLE FOR DIARRHEA IN AN ACUTE VIRAL ENTERITIS IN PIGLETS
TRANSMISSIBLE GASTROENTERITIS - MECHANISMS RESPONSIBLE FOR DIARRHEA IN AN ACUTE VIRAL ENTERITIS IN PIGLETS
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DOI：
10.1172/jci107681
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发表时间：
1974-01-01
影响因子：
15.9
通讯作者：
HAMILTON, JR
中科院分区：
文献类型：
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作者：
BUTLER, DG;GALL, DG;HAMILTON, JR
本研究在实验感染传染性胃肠炎(TGE)病毒40h后，对3周龄仔猪进行了研究，以确定该病的腹泻机制，并更好地了解人类感染性腹泻。在肠道的四个区域使用连续节段性标记灌流，我们发现只有在空肠近端，即病毒感染的区域，腔内净积水和电解质显著增加。在活体研究的空肠段中，与配种仔猪相比，单向钠流量、细胞外液(ECF)到管腔的流量显著增加，管腔到ECF的流量显著降低。在正常猪的同一节段加入甘露醇(450摩尔/公斤)造成高张标准灌流液，仅引起ECF对管腔钠通量的增加。TGE不改变大体绒毛结构或管腔内细菌、胆盐、乳酸、pH或渗透压。感染猪空肠上皮细胞迁移加快。在悬浮液中分离的TGE猪的这些细胞表现出主动和被动的钠外流增加，而甘露醇灌流的猪的细胞只表现出主动的钠外流增加。在这种病毒性肠炎中，发生在空肠的钠转运改变，肠道感染区域似乎与上皮细胞功能缺陷有关。钠转运异常的确切性质，它们与其他溶质转运障碍的关系，以及与病毒上皮细胞相互作用的关系仍有待确定。
We studied 3-wk-old piglets 40 h after experimental infection with transmissible gastroenteritis (TGE) virus to identify the mechanisms of diarrhea in this disease and to better understand infectious diarrhea in humans. Using continuous segmental marker perfusion in four regions along the gut, we found significant increases in net intraluminal accumulation of water and electrolytes only in the proximal jejunum, the region infected by the virus. In this jejunal segment studied in vivo, unidirectional sodium flux, extracellular fluid (ECF) to lumen, significantly increased, lumen to ECF significantly decreased, compared with matchfed littermates. The standard perfusate rendered hypertonic by adding mannitol (450 mosmol/kg), in the same segment of normal pigs, caused only an increase in ECF to lumen flux of sodium. TGE did not alter gross villous structure or intraluminal bacteria, bile salts, lactate, pH, or osmolality. Epithelial cell migration was accelerated in the jejunum of infected pigs. Isolated in suspension, these cells from TGE pigs exhibited increased active and passive sodium efflux, cells from mannitol-perfused pigs exhibited only increased active sodium efflux. In this viral enteritis, altered sodium transport occurring in the jejunum, the region of the intestine infected appears to be associated with defective epithelial cell function. The precise nature of the abnormalities in sodium transport, their relationship to disturbances of transport of other solutes, and to virus epithelial cell interaction remain to be defined.Images