Article ID Journal Published Year Pages File Type
4309870 Surgery 2006 10 Pages PDF
Abstract

BackgroundSeveral experimental studies have shown the beneficial effects of nitric oxide (NO) in the modulation of the systemic inflammatory response syndrome (SIRS). Nitric oxide is involved in and affects almost all stages in the development of inflammation. We have attempted to ascertain whether the nitric oxide donor molsidomine prevents aortic graft contamination through control of the SIRS and a decrease in bacterial translocation (BT).MethodsTwenty-four mini-pigs were divided into 4 groups. The animals were subjected to suprarenal aortic/iliac cross-clamping (for 30 minutes) and by-pass with a Dacron-collagen prosthetic graft impregnated in rifampicin. Groups: 1) sham (aortic dissection alone); 2) cross-clamping and bypass; 3) hemorrhage of 40% of total blood volume before cross-clamping and by-pass; and 4) the same as in group 3 but also including the administration of the NO donor molsidomine (4 mg/kg) 5 minutes before cross-clamping. Variables: 1) bacteriology of mesenteric lymph nodes (MLN), kidney, blood, and prosthesis; 2) serum TNF-α (ELISA); and 3) iNOS expression in kidney and liver (Western blot).ResultsAortic cross-clamping with or without hemorrhage was associated with BT in 80% and 100% of the animals, respectively. About 86% of the bacteria isolated in the graft were also present in MLN. This contamination coincided with an increase in TNF-α and with a greater expression of iNOS. Molsidomine administration decreased TNF-α and iNOS, decreased BT (from 100% to 20% of the animals), and decreased graft contamination (from 83% to 20%).ConclusionsThe present model induces high levels of BT and SIRS, both acted as sources of contamination for the implanted Dacron graft. Molsidomine administration decreased the presence of bacteria in the graft by controlling BT and modulating SIRS.

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