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The influence of the CO2 pneumoperitoneum on a rat model of intestinal anastomosis healing
The influence of the CO2 pneumoperitoneum on a rat model of intestinal anastomosis healing
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The influence of the CO2 pneumoperitoneum on a rat model of intestinal anastomosis healing
The influence of the CO2 pneumoperitoneum on a rat model of intestinal anastomosis healing

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The influence of the CO2 pneumoperitoneum on a rat model of intestinal anastomosis healing
The influence of the CO2 pneumoperitoneum on a rat model of intestinal anastomosis healing
Journal Article

The influence of the CO2 pneumoperitoneum on a rat model of intestinal anastomosis healing

2012
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Overview
Background The CO 2 pneumoperitoneum, which is used for laparoscopic surgery, causes local and systemic effects in patients. Concern arises about what the pressurized anoxic environment of the CO 2 pneumoperitoneum has on intestinal healing. Earlier experimental work showed a negative correlation between intestinal healing and the applied intra-abdominal pressure. To further elucidate this, we developed a rat model, in which enterotomy healing can be compared after open or laparoscopic surgery. Possible mechanisms of injury, such as impaired neoangiogenesis or injury through hypoxia-induced pathways were studied. Methods A new experimental mechanically ventilated rat model was developed. An enterotomy was made and closed via laparotomy (group I) or laparoscopy under CO 2 pressures of 5 mmHg (group II) or 10 mmHg (group III). Intestinal healing was tested in vivo after 1 week by bursting-pressure analysis. The effect of the operative procedure on neoangiogenesis was tested by counting factor VIII positive vessels in biopsies of the perianastomotic granulation tissue after 1 week. Intestinal anoxia was tested by quantifying HIF-1α protein levels in intestinal biopsies, taken before the enterotomy closure. Results The bursting pressures were significantly lower after laparoscopic surgery at 10 mmHg CO 2 pneumoperitoneum (group III) compared with rats that had undergone open surgery (group I) or laparoscopic surgery at 5 mmHg CO 2 pneumoperitoneum (group II). There was no significant quantitative difference between the three groups in the neoangiogenesis nor was there a difference in the amount of HIF-1α measured in the intestinal biopsies. Conclusions We developed a surgical model that is well fitted to study the effects of pneumoperitoneum on intestinal healing. With this model, we found further evidence of CO 2 pressure-dependant hampered intestinal healing. These differences could not be explained by difference in neoangiogenesis nor local upregulation of hypoxic factors.