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 lymp hocytes in vitro we decided to investigate lymphocyte stress during la paroscopy. Blood samples and peritoneal fluids mere obtained before an d after pneumoperitoneum from 16 patients undergoing laparoscopic chol ecystectomy. Lymphocyte subsets were determined by flow cytometry. Pro pidium iodide was used as a lymphocyte vitality test, Cytokines were m easured by an ELISA system. Significant falls in the absolute lymphocy te count and T3 and T4 lymphocytes occurred on postoperative day 1 wit h a quick return to the preoperative value on day 2. T8, natural kille r cells, T4/T8, and T4(+)/T8(+) counts were stable. Interleukins 1 bet a and 6 and tumor necrosis factor-alpha were depressed during the two postoperative days. Peritoneal lymphocytes were not destroyed by pneum operitoneum as demonstrated by the propidium test, nor were they local ly impaired by carbon dioxide. The circulating lymphocyte subpopulatio n decrease favors moderate, brief immunodepression. The origin of port site metastases is not immunologic depression but, rather, facilitate d implantation of malignant cells by hyperpressure into raw tissues.