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

Abstract

BackgroundThe CO2 pneumoperitoneum, which is used for laparoscopic surgery, causes local and systemic effects in patients. Concern arises about what the pressurized anoxic environment of the CO2 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.MethodsA new experimental mechanically ventilated rat model was developed. An enterotomy was made and closed via laparotomy (group I) or laparoscopy under CO2 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.ResultsThe bursting pressures were significantly lower after laparoscopic surgery at 10 mmHg CO2 pneumoperitoneum (group III) compared with rats that had undergone open surgery (group I) or laparoscopic surgery at 5 mmHg CO2 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.ConclusionsWe 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 CO2 pressure-dependant hampered intestinal healing. These differences could not be explained by difference in neoangiogenesis nor local upregulation of hypoxic factors.