Abstract
Net intestinal transport of sodium in vivo, in control and enterotoxin (Clostridium perfringens)-treated rats, was resolved into two unidirectional fluxes, influx from and efflux into the lumen of the terminal ileum. In rats treated with the toxin, sodium influx remained similar to control values even during fluid and electrolyte loss to the lumen. Net loss of sodium was shown to be due to nearly a twofold increase in sodium efflux to the lumen in toxin-treated animals. There was only slight histopathological damage to the mucosa, especially noticeable at the tips of villi.
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