These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Effect of Shigella enterotoxin on electrolyte transport in rabbit ileum.
    Author: Donowitz M, Keusch GT, Binder HJ.
    Journal: Gastroenterology; 1975 Dec; 69(6):1230-7. PubMed ID: 172398.
    Abstract:
    Shigella dysenteriae I is one of several bacteria which produces an enterotoxin capable of stimulating intestinal water and electrolyte secretion. Unlike cholera and Escherichia coli enterotoxins which have been shown to increase intracellular cyclic adenosine monophosphate levels in the small intestine, the mechanism by which shigella enterotoxin causes intestinal secretion is not known. To study shigella enterotoxin-stimulated intestinal secretion, rabbit ileal mucosa exposed in vivo to Shigella dysenteriae I enterotoxin was studied in vitro in a modified Ussing chamber. Fluid and electrolyte accumulation occurred in vivo and net sodium secretion was present in vitro in the enterotoxin-exposed tissue in contrast to net sodium absorption in control mucosa. Short-circuit current (Isc) was similar in shigella enterotoxin-exposed tissue compared with control tissue. The increase adenosine monophosphate was similar to enterotoxin-exposed and control mucosa. The addition of glucose resulted in a smaller increment of Isc in shigella enterotoxin-treated tissue. Mucosal cyclic adenosine monophosphate levels in enterotoxin-exposed mucosa did not differ from those of control. These results indicate that the characteristics of rabbit ileal mucosa exposed to shigella enterotoxin and cholera enterotoxin markedly differ, although both produce electrolyte secretion both in vivo and in vitro. These studies further suggest that, in contrast to its role in cholera enterotoxin-induced intestinal secretion, cyclic adenosine monophosphate may not be in the mediator of shigella enterotoxin stimulation of intestinal fluid and electrolyte secretion.
    [Abstract] [Full Text] [Related] [New Search]