Objective: To investigate the effects of CO(2) insufflation with different pressures upon the injury, proliferation and secretion of peritoneal mesothelial cells and the possible effects of gastric cancer cells adhering to mesothelial cells.
Methods: Primary cultured peritoneal mesothelial cells were divided into CO(2) and control group. In CO(2) group, the cells were exposed to CO(2) at different pressures (10, 12 and 15 mm Hg). And then the cellular injury was detected by LDH assay, the proliferation quantified by MTT assay and the secretion measured by ELISA. Flow cytometry was used to analyze the adherent rate between gastric cancer cells and mesothelial cells.
Results: The LDH assay showed that 10 and 12 mm Hg subgroups were not significantly different from that in the control group (P > 0.05) whereas the 15 mm Hg subgroup was higher than the control group (122.79 +/- 4.28 vs 100.89 +/- 1.22, P < 0.05). MTT assay indicated that 10 and 12 mm Hg subgroups were similar to that of the control group (P > 0.05). However the 15 mm Hg subgroup decreased to 1.08 +/- 0.05 at 72 h post-experiment. But the same finding was not observed during first 48 h. The concentration of IL-6 in each group increased as compared with the control group (1.21 +/- 0.05, P < 0.05). Moreover this tendency was persistent only in the 15 mm Hg subgroup (P < 0.05). The results of flow cytometry showed that the adherent rate between gastric cancer cells and mesothelial cells in each CO(2) group were similar to the control group (all P > 0.05).
Conclusion: Pressures of CO(2) at 10 and 12 mm Hg have no effect upon the injury and proliferation of peritoneal mesothelial cells. When pressure rises to 15 mm Hg, the cellular injury becomes apparent and the proliferation is inhibited. The CO(2) environment up-regulates the level of IL-6. It may benefit to the local immune reaction of peritoneum. The CO(2) pneumoperitoneum does not promote the adhesion of gastric cancer cells to mesothelial cells.
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