Influence of CO2 pneumoperitoneum on systemic and peritoneal cell-mediated immunity

Port site metastases could be due to mechanical reasons or impairment of host defenses. As it is known that carbon dioxide is toxic for lymphocytes in vitro we decided to investigate lymphocyte stress during laparoscopy. Blood samples and peritoneal fluids were obtained before and after pneumoperitoneum from 16 patients undergoing laparoscopic cholecystectomy. Lymphocyte subsets were determined by flow cytometry. Propidium iodide was used as a lymphocyte vitality test. Cytokines were measured by an ELISA system. Significant falls in the absolute lymphocyte count and T3 and T4 lymphocytes occurred on postoperative day 1 with a quick return to the preoperative value on day 2. T8, natural killer cells, T4/T8, and T4+/T8+ counts were stable. Interleukins 1 beta and 6 and tumor necrosis factor-alpha were depressed during the two postoperative days. Peritoneal lymphocytes were not destroyed by pneumoperitoneum as demonstrated by the propidium test, nor were they locally impaired by carbon dioxide. The circulating lymphocyte subpopulation decrease favors moderate, brief immunodepression. The origin of port site metastases is not immunologic depression but, rather, facilitated implantation of malignant cells by hyperpressure into raw tissues.