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Am J Physiol Heart Circ Physiol (September 11, 2003). doi:10.1152/ajpheart.00234.2003
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Submitted on March 18, 2003
Accepted on September 8, 2003

Effect of Nitric Oxide on Capillary Hemodynamics and Cell Injury in the Pancreas during Pseudomonas Pneumonia Induced Sepsis

Barbara Tribl1*, Ryon M. Bateman2, Stephanie Milkovich2, William J. Sibbald3, and Christopher G. Ellis2

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

* To whom correspondence should be addressed. E-mail: barbara.tribl{at}akh-wien.ac.at.

Sepsis induced nitric oxide 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 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 hours following induction of pneumonia. With pneumonia plasma nitrite/nitrate (NO2-/NO3- or NOx-) levels were doubled by 21 hours (p<0.05). To assess the effect of NO overproduction on microvascular perfusion, L-N6-(1-iminoethyl) lysine (L-NIL) was administered to maintain NOx- levels at baseline. Pneumonia did cause a decrease in RBC velocity of 23% by 6-hours but by 24 hours RBC velocity and supply rate had increased relative to sham by 22% and 38% respectively (p<0.05). LNIL 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.




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J. H. Crawford, B. K. Chacko, H. M. Pruitt, B. Piknova, N. Hogg, and R. P. Patel
Transduction of NO-bioactivity by the red blood cell in sepsis: novel mechanisms of vasodilation during acute inflammatory disease
Blood, September 1, 2004; 104(5): 1375 - 1382.
[Abstract] [Full Text] [PDF]


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