Peritoneal host defenses: modulation by carbon dioxide insufflation

The host response to inflammatory stimuli in the peritoneal cavity consists of coordinated interactions of physical factors, cells, and soluble mediator molecules. Following infection, this is characterized by rapid eradication of large numbers of bacteria via the diaphragmatic lymphatics, clearance of bacteria through phagocytosis and intracellular killing, and, finally, sequestration of residual bacteria by inflammatory fibrinous exudate. Increasingly, surgical infections and major operations with the potential for postoperative infection are being managed laparoscopically, with CO(2) insufflation. The effects of CO(2) on intraperitoneal host defenses are still being defined.

Review of the pertinent literature and results from our laboratory.

Exposure of peritoneal macrophages in vitro to CO(2) causes intracellular acidification, which in turn suppresses production of tumor necrosis factor (TNF) in response to exposure to lipopolysaccharide (LPS). In comparison, neither room air nor helium had any effect on cytosolic pH or the peritoneal macrophage response to LPS. Insufflation of CO(2) into the preperitoneal space in vivo caused similar peritoneal lining acidosis and reduced TNF production compared with insufflation of helium.

CO(2) pneumoperitoneum created during laparoscopy appears to exert immunosuppressive effects through its ability to acidify the intracellular compartment of inflammatory cells. This may contribute to the improved recovery in patients undergoing laparoscopic surgery.