Microvascular perfusion deficits are not a prerequisite for mucosal injuryin septic rats

Our major objective was to investigate whether injury to the mucosa of the small intestine occurred in a normotensive model of sepsis and whether such injury was associated with microvascular perfusion deficits. Using fluores cence intravital microscopy, we show direct evidence of cell injury within the mucosa (pneumonia 12.4 +/- 2.6 cells/field, sham 2.2 +/- 0.7 cells/fiel d), whereas use of Cr-51-labeled EDTA showed evidence of increased mucosal permeability (pneumonia 1.90 +/- 0.67 ml.min(-1).100 g(-1); sham 0.24 +/- 0 .04 ml.min(-1).100 g(-1)), 48 h following induction of pneumonia. Despite s uch injury the capillary density in the ileal mucosa and submucosa of pneum onic rats (1,027 +/- 77 and 1,717 +/- 86 mm(2)) was not significantly diffe rent compared with sham (998 +/- 63 and 1,812 +/- 101 mm(2)). However, a mo dest albeit significant decrease in capillary perfusion was measured in the muscularis layer of pneumonia (11.0 +/- 1.3 mm) compared with sham (13.9 /- 0.63 mm) and appeared to be associated with leukocyte entrapment. Pretre atment using low doses of endotoxin to induce endotoxin tolerance not only increased muscularis capillary density but reduced the number of leukocytes trapped within the microvasculature, decreased myeloperoxidase activity wi thin the ileum in pneumonic rats, and prevented mucosal injury. In conclusi on, we have shown that pneumonia results in remote injury to the mucosa of the ileum and that such injury was not associated with concurrent mucosal p erfusion deficits.