Microcirculator yDysfunctio ni nEndotoxemi cBowe lAnastomosis :The Pathogeneti cContributio no fMicrocirculator yDysfunctio nto Endotoxemia-Induce dHealin gImpairment

Background. An established intra-abdominal infection as in perforated diverticulitis is considered to contribute to anastomotic healing impairment. Since microvascular dysfunction in sepsis is known to be due to organ failure, the influence of inflammation on the anastomotic microcirculation needs further investigation. Material and methods. Sixty BALB/c mice (n 10 per group a n d d a y 2 , 4 , a n d 7 ) w e r e randomized to two groups: Control and Sepsis (lipopolysaccharide administration 2 mg/kg bodyweight 18 h before colon surgery). All animals underwent colonic anastomosis. Immediately after its completion intravital fluorescence microscopy of the anastomosis was performed, and both macroscopic and histological parameters were assessed on days 2, 4, and 7 postoperatively. Additionally, immunohistology was performed for CD31 (platelet endothelial cell adhesion molecule-1), single-strand DNA, and inducible nitric oxide synthase. Results. As compared to Control the functional capillary network of the perianastomotic region was decreased in Sepsis (P < 0.001) as well as the hemoglobin O2 saturation in the antimesenteric region of the anastomosis (P < 0.05). Bursting pressure was significantly decreased in Sepsis compared to Control at days 2, 4, and 7. On day 7 there were significant differences between the two groups in the anastomotic region: neutrophil infiltration in Sepsis was higher (P < 0.001); vascular density and differentiation in Sepsis was lower (P < 0.01, P < 0.05, respectively); and apoptosis was higher in Sepsis (P < 0.05). Conclusion. The inflammatory state increases microvascular dysfunction at the anastomosis resulting in