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Effect of nitric oxide on capillary hemodynamics and cell injury in the pancreas during Pseudomonas pneumonia-induced sepsis

¹Sunnybrook and Women's College Health Sciences Centre, University of Toronto, Toronto M4N 3M5; and ²Lawson Health Research Institute and Department of Medical Biophysics, University of Western Ontario, London, Ontario, Canada N6A 5B8

Submitted 18 March 2003 ; accepted in final form 8 September 2003

Sepsis-induced nitric oxide (NO) overproduction has been implicated in a redistribution of flow from the pancreas making it vulnerable to ischemic injury in septic shock. To test this hypothesis in a remote injury model of normotensive sepsis, we induced Pseudomonas pneumonia in the rat and used intravital video microscopy (IVVM) of the pancreas to measure functional capillary density, capillary hemodynamics [red blood cell (RBC) velocity, lineal density, and supply rate], and lethal cellular damage (propidium iodine staining) at 6 and 24 h after the induction of pneumonia. With pneumonia, plasma nitrite/nitrate [] levels were doubled by 21 h (P < 0.05). To assess the effect of NO overproduction on microvascular perfusion, N⁶-(1-iminoethyl)-L-lysine (L-NIL) was administered to maintain levels at baseline. Pneumonia did cause a decrease in RBC velocity of 23% by 6 h, but by 24 h RBC velocity and supply rate had increased relative to sham by 22 and 38%, respectively (P < 0.05). L-NIL treatment demonstrated that this increase was due to NO overproduction. With pneumonia, there was no change in functional capillary density and only modest increases in cellular damage. We conclude that, in this normotensive pneumonia model of sepsis, NO overproduction was protective of microvascular perfusion in the pancreas.

sepsis syndrome; bacterial pneumonia; microcirculation

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