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Charles C. J. Carpenter, R. Bradley Sack, John C. Feeley, Richard W. Steenberg
J Clin Invest. 1968;
47(5):1210
doi:10.1172/JCI105810
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he site and characteristics of gastrointestinal electrolyte loss were investigated in eight dogs with experimental cholera induced by orogastric administration of 6-hr broth cultures of Vibrio cholerae, strain Ogawa 395. In these animals, all electrolyte losses originated in the small bowel, predominantly from the jejunum and ileum. The bicarbonate concentration of the small bowel fluid showed a progressive increase from duodenum, where it was less than that of plasma, to the terminal ileum, where it was significantly greater than that of simultaneously obtained plasma.Studies of the responses of chronic Thiry-Vella jejunal loops (five dogs) and chronic Thiry-Vella ileal loops (five dogs) to intraluminal challenge by cholera exotoxin demonstrated that all loops exhibited isotonic electrolyte loss for a 14-18 hr period after challenge. The bicarbonate concentration of fluid produced by exotoxin-challenged jejunal loops was not significantly different from that of plasma, whereas the ileal loops produced fluid with a bicarbonate concentration approximately three times that of plasma.The effect of intraluminal glucose on the response of canine gut to cholera exotoxin was investigated by perfusion studies in 12 dogs with chronic Thiry-Vella fistulae. Intraluminal glucose significantly enhanced isotonic fluid absorption in both jejunal and ileal loops. The net effects of glucose on isotonic fluid absorption were equal before and after intraluminal administration of crude cholera exotoxin. These data suggest that cholera exotoxin causes gut electrolyte loss by a mechanism independent of that by which glucose enhances sodium absorption.
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