Carbon dioxide pneumoperitoneum–mediated attenuation of the inflammatory response is independent of systemic acidosis

Abstract

The purpose of this study was to determine if systemic acidosis induced by peritoneal absorption of carbon dioxide (CO2 ) during laparoscopy plays a role in CO2 pneumoperitoneum-mediated attenuation of the acute phase inflammatory response associated with perioperative sepsis. The influence of hepatic polymorphonuclear (PMN) leukocyte infiltration on this phenomenon was also investigated. Forty-five rats were randomized into 5 groups: anesthesia control, open cecal ligation and puncture (OCLP), laparoscopic cecal ligation and puncture using helium for insufflation (He LCLP), LCLP using CO2 with continued spontaneous ventilation (LCLP-SV), and LCLP using CO2 with intubation and positive pressure ventilation (LCLP-PPV). After 30 minutes, arterial blood gas parameters remained normal in control, OCLP rats, and He LCLP rats, while CO2 LCLP-SV rats developed significant hypercarbic acidosis. This acidosis was corrected in CO2 LCLP-PPV rats ( P < .0001 vs CO2 LCLP-SV for both). Expression of the rat acute phase gene alpha 2 -macroglobulin was greater after OCLP and He LCLP than after either CO2 LCLP-SV or CO2 LCLP-PPV ( P < .0001 vs either CO2 OCLP-SV for both). However, levels of alpha 2 -macroglobulin were not significantly different between the acidotic (LCLP-SV) and normocarbic (LCLP-PPV) CO2 groups. Infiltration of the hepatic parenchyma by PMNs did not differ significantly between groups. CO2 insufflation-induced systemic acidosis is not responsible for the reduction in the acute phase inflammatory response observed in laparoscopic animal models of sepsis. Hepatic PMN infiltration also does not appear to mediate this effect.