Modeling open surgery in mice to explore peritoneal damage, carbon dioxide humidification and desmoidogenesis

Summary

To explore the role of open and laparoscopic surgery in the process of desmoidogenesis we crossed Apcmin/ +C57Bl/6 mice with p53 +/- mice to generate animals that developed desmoid tumors with 100% penetrance. One hour of active airflow generates substantial damage to peritoneal mesothelial cells and their microvilli as measured at 24?h post intervention, which is significantly greater than that generated by passive airflow. Use of humidified-warm CO2 mostly protects the mesothelium that had not experienced additional mechanical (surgical) damage at 24?h. Maximal damage was evident in all treatment groups regardless of flow or use of gas. At day 10 mechanically-damaged peritoneum remains in mice but is essentially repaired in the gas-treated groups. Regarding desmoidogenesis, operating procedures did not increase the frequency of desmoid tumors but their frequency correlated with time following surgery but not age of mice. Active airflow generates more peritoneal damage than passive airflow and is reduced significantly by the use of humidified-warm CO2. Introduced peritoneal damage is largely repaired in mice by day 10 with gas. Desmoid tumor incidence is not increased substantially by surgery itself but rises over time following surgery compared to non-surgery mice.