Acta cirurgica brasileira · 2009
Bacterial translocation in an experimental intestinal obstruction model. C-reactive protein reliability?
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El-Awady Saleh Ibrahim, El-Nagar Mohammed, El-Dakar Medhat, Ragab Mohammed, Elnady Ghada
Аннотация
BACKGROUND: Bacterial translocation occurs in preseptic conditions such as intestinal obstruction through unclear mechanism. The C-reactive protein is an acute phase reactant and a marker of ischemia.
METHODS: 45 albino male rats were divided into 3 groups each 15 rats. GI control, GII simple intestinal-obstruction and GIII strangulated obstruction. Outcome measures were: (1) Bacteriologic count and typing for intestinal contents, intestinal wall, liver, mesenteric lymph nodes and blood (cardiac and portal) (2) Histopathologic: mucosal injury score, inflammatory cell infiltrate in the wall, MLN, liver, (3) Biochemical: serum CRP, IL-10, mucosal stress pattern (glutathione peroxidase-malonyldialdhyde tissue levels).
RESULTS: (1) Intestinal obstruction associates with BT precursors (Bact-overgrowth, mucosal-acidosis, immuno-incomptence), (2) Bacterial translocation (frequency and density) was found higher in strangulated I.O, that was mainly enteric (aerobic and anaerobic) and mostly E.coli, (3) The pathogen commonality supports the gut origin hypothesis but the systemic inflammatory response goes with the cytokine generating one. (4) The CRP median values for GI, II, III were 0.5, 6.9, 8.5 mg/L, for BT +ve 8 mg/L and 0.75 mg/L for BT -ve rats.
CONCLUSION: Bacterial translocation occurs bi-directional (systemic-portal) in intestinal obstruction and the resultant inflammatory response pathogenesis is mostly 3 hit model. The CRP is a non selective marker of suspected I.O cases. However, it is a reliable marker of BT, BT density and vascular compromise during I.O.
METHODS: 45 albino male rats were divided into 3 groups each 15 rats. GI control, GII simple intestinal-obstruction and GIII strangulated obstruction. Outcome measures were: (1) Bacteriologic count and typing for intestinal contents, intestinal wall, liver, mesenteric lymph nodes and blood (cardiac and portal) (2) Histopathologic: mucosal injury score, inflammatory cell infiltrate in the wall, MLN, liver, (3) Biochemical: serum CRP, IL-10, mucosal stress pattern (glutathione peroxidase-malonyldialdhyde tissue levels).
RESULTS: (1) Intestinal obstruction associates with BT precursors (Bact-overgrowth, mucosal-acidosis, immuno-incomptence), (2) Bacterial translocation (frequency and density) was found higher in strangulated I.O, that was mainly enteric (aerobic and anaerobic) and mostly E.coli, (3) The pathogen commonality supports the gut origin hypothesis but the systemic inflammatory response goes with the cytokine generating one. (4) The CRP median values for GI, II, III were 0.5, 6.9, 8.5 mg/L, for BT +ve 8 mg/L and 0.75 mg/L for BT -ve rats.
CONCLUSION: Bacterial translocation occurs bi-directional (systemic-portal) in intestinal obstruction and the resultant inflammatory response pathogenesis is mostly 3 hit model. The CRP is a non selective marker of suspected I.O cases. However, it is a reliable marker of BT, BT density and vascular compromise during I.O.