title: Bacterial translocation as a source of Dacron-graft contamination in experimental aortic operation: the importance of controlling SIRS.
abstract: BACKGROUND
  Several 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).
  
  
  METHODS
  Twenty-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.
  
  
  METHODS
  1) bacteriology of mesenteric lymph nodes (MLN), kidney, blood, and prosthesis; 2) serum TNF-alpha (ELISA); and 3) iNOS expression in kidney and liver (Western blot).
  
  
  RESULTS
  Aortic 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-alpha and with a greater expression of iNOS. Molsidomine administration decreased TNF-alpha and iNOS, decreased BT (from 100% to 20% of the animals), and decreased graft contamination (from 83% to 20%).
  
  
  CONCLUSIONS
  The 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.
authors.affiliation: Service of Vascular Surgery, Salamanca, Spain; Experimental Surgery Unit, Medical School, University of Salamanca, Spain.
authors.forename: Francisco S
authors.initials: FS
authors.lastname: Lozano
authors.forename: Carlos
authors.initials: C
authors.lastname: Cascajo
authors.forename: Enrique
authors.initials: E
authors.lastname: García-Sánchez
authors.forename: Marcello B
authors.initials: MB
authors.lastname: Barros
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: García-Criado
authors.forename: Felipe
authors.initials: F
authors.lastname: Parreño
authors.forename: José Elias
authors.initials: JE
authors.lastname: García-Sánchez
authors.forename: Alberto
authors.initials: A
authors.lastname: Gómez-Alonso
mesh_terms: D000818:Animals; D001011:Aorta / Q000601:surgery*; D001419:Bacteria / Q000302:isolation & purification* / Q000472:pathogenicity; D001693:Biological Transport, Active; D001807:Blood Vessel Prosthesis / Q000009:adverse effects*; D019917:Blood Vessel Prosthesis Implantation / Q000009:adverse effects / Q000379:methods; D007668:Kidney / Q000187:drug effects / Q000201:enzymology; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D008297:Male; D008981:Molsidomine / Q000494:pharmacology; D020030:Nitric Oxide Donors / Q000494:pharmacology; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D011093:Polyethylene Terephthalates; D013552:Swine; D013556:Swine, Miniature; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000382:microbiology / Q000517:prevention & control*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D020030:Nitric Oxide Donors; D011093:Polyethylene Terephthalates; D014409:Tumor Necrosis Factor-alpha; D008981:Molsidomine; D052247:Nitric Oxide Synthase Type II