Endotoxin-induced ileal XXXX in @entity1707 : role of tissue @entity520 .

@entity1707 @entity63 @entity33 @entity2822 @entity520 @entity519 @entity880 @entity5327
Administration of lipopolysaccharide (LPS) to experimental animals leads to diminished mesenteric perfusion, increased ileal mucosal [H+] , and increased gut epithelial permeability to hydrophilic solutes. We sought to determine whether these phenomena are causally related. Experiments were performed in anesthetized @entity1707 . Permeability was assessed by measuring the plasma-to-lumen clearance of @entity2822 dextran (4,000 Da; FD-4) by a segment of ileum perfused with Ringer lactate solution. Mucosal perfusion (Qmuc) and [H4+] were estimated using laser-Doppler flowmetry and tonometry, respectively. In an initial series of experiments, we showed that mucosal permeability was linearly correlated with mucosal [H+] in animals subjected to graded degrees of mechanically induced @entity5327 (n = 14, R2 = 0.58, P < 0.002) or injected with graded doses of LPS (n = 11, R2 = 0.93, P < 0.0001). In a second series of experiments, we induced @entity33 in normal @entity1707 by mechanical ventilation with either a @entity519 (n = 7) or a hypercapnic (n = 5) gas mixture. In both groups, ileal mucosal permeability to FD-4 increased significantly (P < 0.05), although transmesenteric release of @entity880 increased significantly only in the @entity519 group. Qmuc was unchanged in both groups. These data suggest that @entity33 , even in the absence of tissue @entity63 or @entity519 , increases intestinal permeability to a macromolecular hydrophilic solute. Tissue @entity520 may be an important factor contributing to LPS-induced gut @entity33 .
