Microcirculatory dysfunction in endotoxemic bowel anastomosis: the pathogenetic contribution of microcirculatory
Ricarda Diller1, Udo Stratmann, Tilo Helmschmied
1Surgical Research, Department of General Surgery-University Hospital of Münster, Münster, Germany. diller@uni-muenster.de
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 and day 2, 4, and 7) were 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 O(2) 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 healing impairment.
Insights
Sepsis-induced inflammation impairs colonic anastomosis healing by causing microvascular dysfunction. This study shows reduced capillary networks and oxygen saturation, leading to lower bursting pressure and impaired healing in septic mice.
Area of Science:
- Surgical innovation
- Gastroenterology
- Inflammation and immunology
Background:
- Intra-abdominal infections, such as perforated diverticulitis, can impede anastomotic healing.
- Sepsis-related microvascular dysfunction is a known cause of organ failure, but its impact on anastomotic microcirculation requires further study.
Purpose of the Study:
- To investigate the influence of inflammation on anastomotic microcirculation and healing in a sepsis model.
- To assess the effects of sepsis on the functional capillary network, vascular density, and tissue integrity at the site of colonic anastomosis.
Main Methods:
- A murine model of colonic anastomosis was established in control and sepsis-induced (lipopolysaccharide administration) BALB/c mice.
- Intravital fluorescence microscopy, macroscopic, and histological assessments were performed on postoperative days 2, 4, and 7.
- Immunohistology was utilized to evaluate markers of vascularity (CD31), apoptosis, and neutrophil infiltration.
Main Results:
- Sepsis significantly reduced the functional capillary network and hemoglobin O(2) saturation in the anastomotic region.
- The bursting pressure of colonic anastomoses was significantly lower in septic mice compared to controls.
- On postoperative day 7, septic anastomoses exhibited increased neutrophil infiltration, decreased vascular density and differentiation, and higher apoptosis rates.
Conclusions:
- The inflammatory state associated with sepsis exacerbates microvascular dysfunction at the anastomosis.
- This microvascular dysfunction directly contributes to impaired anastomotic healing and reduced tissue integrity.
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