Endotoxin inhibitor prevents sepsis-induced alterations in intestinal ion transport.
BACKGROUND
The intestine is a target of septic insult. The aims of this study were to characterize sepsis-induced alterations in intestinal ion transport and to determine the role endotoxin plays in mediating these changes.


METHODS
Rats underwent cecal manipulation alone (control), cecal ligation and puncture (CLP), or CLP plus intraperitoneal injection of 0.2 mg of a recently synthesized endotoxin inhibitor. At 24 hours, distal ileum was harvested, and transport parameters were determined.


RESULTS
Cecal ligation and puncture produced a significant increase in short-circuit current (Isc) that was attributable to the induction of chloride secretion. There were no alterations in transepithelial resistance or fluxes of mannitol and sodium. The sepsis-induced increase in Isc was prevented by administration of the endotoxin inhibitor.


CONCLUSIONS
In this model of sepsis, the primary alteration in ileal ion transport is an induction of electrogenic chloride secretion. Endotoxin inhibition may represent a strategy for prophylaxis against the intestinal effects of sepsis.
Whang
E E
EE
Department of Surgery, UCLA School of Medicine, USA.
Dunn
J C
JC
Mahanty
H
H
McFadden
D W
DW
Zinner
M J
MJ
Ashley
S W
SW
D000818:Animals; D002432:Cecum / Q000293:injuries / Q000601:surgery; D004195:Disease Models, Animal; D004731:Endotoxins / Q000037:antagonists & inhibitors*; D004751:Enteritis / Q000378:metabolism*; D066298:In Vitro Techniques; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism*; D017136:Ion Transport / Q000187:drug effects; D008026:Ligation; D010539:Permeability / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley
D004731:Endotoxins