Microvascular perfusion deficits are not a prerequisite for mucosal injury in 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 fluorescence intravital microscopy, we show direct evidence of cell injury within the mucosa (pneumonia 12.4 +/- 2.

Leukocyte activation and flow behavior in rat skeletal muscle in sepsis.

In animal models of endotoxemia, sepsis is associated with the accumulation of leukocytes and altered microvascular perfusion. In order to test the hypothesis that bacterial sepsis upregulates leukocyte-endothelial adhesion, we used intravital microscopy to examine the flow behavior of leukocytes in the postcapillary venules (PCV) of rats made septic by cecal ligation and perforation (CLP). Animals were randomized to CLP or sham study groups and studied 6 h, 24 h, or 48 h later.

Microcirculatory changes in rat skeletal muscle in sepsis.

The aim of this study was to confirm that microvascular perfusion was abnormal during the early phases of normotensive sepsis and to determine whether these changes were due to the development of tissue edema. Skeletal muscle red blood cell (RBC) flow was studied in rats made septic by cecal ligation and perforation (CLP). After anesthesia with halothane, arterial and venous cannulae were inserted and, in the treatment group, a CLP performed.