McClung H J, Butler D G, Kerzner B, Gall D G, Hamilton J R
Gastroenterology. 1976 Jun;70(6):1091-5. doi: 10.1016/S0016-5085(76)80317-4.
Ion transport in the jejunal mucosa of 14-to 16-day-old piglets with severe diarrhea 40 hr after infection with transmissible gastroenteritis (TGE) virus was studied. In infected pigs Na+ transport failed to respond normally to glucose when studied either in Ussing short-circuited chambers or in suspensions of enterocytes isolated selectively from jejunal villi. Theophylline, 10mM, added to the chambers produced the same brisk electrical responses and increments in net Cl- secretion in tissue from both infected and control groups. A defect in glucose-stimulated Na+ absorption in the acute stage of a viral enteritis has been identified which probably contributes to the impaired lumen-to-extracellular fluid flux of Na+ found previously in the jejunum of intact TGE-infected pigs. The mechanisms causing diarrhea in this invasive viral enteritis differ from those causing toxigenic diarrhea.
研究了感染传染性胃肠炎（TGE）病毒40小时后14至16日龄严重腹泻仔猪空肠黏膜中的离子转运。在感染猪中，无论是在Ussing短路小室中还是在从空肠绒毛中选择性分离的肠上皮细胞悬液中进行研究时，Na⁺转运对葡萄糖均未产生正常反应。向小室中添加10mM的茶碱，在感染组和对照组组织中均产生了相同的强烈电反应以及净Cl⁻分泌增加。已确定病毒性肠炎急性期葡萄糖刺激的Na⁺吸收存在缺陷，这可能是先前在完整感染TGE的猪空肠中发现的Na⁺从肠腔到细胞外液通量受损的原因。这种侵袭性病毒性肠炎导致腹泻的机制与产毒性腹泻的机制不同。
