Increased insufflation pressure enhances the development of liver metastasis in a mouse laparoscopy model: possible mechanisms.

BACKGROUND

The effect of different insufflation pressures and durations of CO2 pneumoperitoneum on the growth of liver metastasis was investigated in a mouse model. The possible mechanisms involved in the pressure-related enhancement of liver metastasis were also examined.

METHODS

Mice inoculated intraportally with colon 26 cells underwent CO2 pneumoperitoneum at different pressures (5,10, or 15 mmHg) for 30 or 60 min, or received no treatment other than tumor cell inoculation (control). The subsequent growth of liver metastases was examined. Mice injected intraportally with 111In-oxine-labeled colon 26 cells underwent pneumoperitoneum at three different pressures or served as controls. The radioactivity of the liver was determined to evaluate tumor accumulation in the liver. Mice received pneumoperitoneum at three different pressures or received trocar placement alone. Changes in plasma interleukin-6 levels were determined.

RESULTS

The growth of liver metastases on day 14 was influenced by increased insufflation pressures (p < 0.05) rather than the prolonged duration of pneumoperitoneum without significant interaction. The 15-mmHg pneumoperitoneum group showed a higher (p < 0.05) accumulation of radioactivity in the liver compared with the 5-mmHg pneumoperitoneum group and controls. Pneumoperitoneum groups with 5 and 10 mmHg showed higher (p < 0.05) peak levels of IL-6 compared with controls.

CONCLUSIONS

An elevated insufflation pressure plays an important role in the enhancement of liver metastases, and this pressure-related adverse effect may be partly relevant to facilitating accumulation of tumor cells in the liver.