CO2 environment influences the growth of cultured human cancer cells dependent on insufflation pressure.

BACKGROUND: Experimental and clinical studies, have suggested that the CO2 pneumoperitoneum influences the development of intraabdominal tumor dissemination and port site metastases. Previous experiments performed both in vitro and in vivo have proved that CO2 insufflation stimulates malignant cell growth. Therefore, we designed a study to investigate the influence of CO2 insufflation administered at different pressures on the growth of cultured human tumor cells. METHODS: Two human tumor cell lines (CX-2 colon adenocarcinoma, DAN-G pancreas adenocarcinoma) were exposed to a CO2 environment maintained at different pressures (0 mmHg, 6 mmHg, 12 mmHg). Tumor growth was determined at different times after exposure to CO2 using fluorescence photometry. Cytotoxity of the CO2 environment different pressures was investigated using flow cytometry. RESULTS: At 1-4 days after exposure to CO2 insufflation, CX-2 and DAN-G tumor cell growth was decreased significantly (p < 0.01). Proliferation of pancreatic adenocarcinoma DAN-G increased significantly from day 5 to day 15 independent of the insufflation pressure (p < 0.01). Proliferation of colon adenocarcinoma CX-2 increased significantly from day 5 to day 15 but was found to be dependent on the insufflation pressure. CX-2 growth increased significantly with higher pressures (p < 0.05). CONCLUSION: CO2 insufflation influences the growth of cultured human tumor cells. After a short period of suppression, the CO2 environment stimulates malignant cell growth. The insufflation pressure may also have additional effects in promoting tumor growth.

[CO2 pneumoperitoneum inhibits in vitro proliferation of human carcinoma cells]. / CO2-Pneumoperitoneum hemmt in-vitro die Proliferation von humanen Karzinomzellen.

Up to this day, the influence of laparoscopy and hyperbaric carbon dioxide on the growth of tumor cells is not yet clear. Cells of human colonic carcinoma CX-2 and pancreatic carcinoma DAN-G were exposed to carbon dioxide under pressures of zero, 6 and 12 mmHg. Proliferation was measured by counting in NEUBAUER's counting chamber and by DNAstaining with Pico Green over five days after exposition. In a third experiment, dead cells were stained with Propidium Iodide and detected by flow cytometry. Only DAN-G after 6 mmHg showed at day five an increasing proliferation rate. Furthermore, exposition to carbon dioxide lead to an increased necrosis of cells. All other groups showed a significantly decreased proliferating activity of the cells exposed to carbon dioxide in comparison to a control group.