title: The effect of a high partial pressure of carbon dioxide environment on metabolism and immune functions of human peritoneal cells-relevance to carbon dioxide pneumoperitoneum.
abstract: OBJECTIVE
  Our purpose was to evaluate in vitro the effect of a high partial pressure of carbon dioxide environment used in laparoscopy on metabolic and immune response of various human peritoneal cells.
  
  
  METHODS
  Polymorphonuclear leukocytes were obtained from 5 healthy volunteers, peritoneal macrophages were obtained from the effluent of 8 patients undergoing continuous ambulatory peritoneal dialysis, and human peritoneal mesothelial cell cultures were prepared from omentum derived from 5 patients undergoing elective surgery. The cells were exposed to a laparoscopy-like environment (1 atmosphere carbon dioxide and 0.2 atmosphere oxygen), to a control gas mixture (1 atmosphere helium and 0.2 atmosphere oxygen), or air for 3 hours. After exposure to gas mixtures, cell functions were tested at various recovery periods.
  
  
  RESULTS
  Three hours of exposure to a high partial pressure of carbon dioxide had no effect on viability of peritoneal macrophages and human peritoneal mesothelial cells, tested by trypan blue dye uptake and lactate dehydrogenase release. A high partial pressure of carbon dioxide decreased the mitochondrial dehydrogenases activity of peritoneal macrophages and human peritoneal macrophage cells by 60%, assayed by 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction. High partial pressure of carbon dioxide blocked the superoxide release from activated polymorphonuclear leukocytes and the secretion of interleukin 1beta from stimulated peritoneal macrophages, and human peritoneal macrophage cells were decreased by 15% and 30% and the secretion of tumor necrosis factor-alpha from peritoneal macrophages was suppressed by 85%. Mitochondrial activity, polymorphonuclear leukocyte function, and interleukin 1beta and tumor necrosis factor-alpha secretion returned to normal after a recovery period of 12 to 24 hours, 4.5 hours, and 24 hours, respectively. In the control experiments exposure of cells to helium had no suppressive effect.
  
  
  CONCLUSIONS
  Exposure of cells to a high partial pressure of carbon dioxide environment suppresses the inflammatory and metabolic responses of peritoneal cells. We suggest that this suppressive effect may contribute to the low postsurgery adhesion formation and the reduction in postoperative pain observed in laparoscopy. Nevertheless, the suppression of the immune response should also be taken into account for operations involving a high risk of bacterial dissemination.
authors.affiliation: Department of Obstetrics and Gynecology "B," Laboratory, and the Department of Nephrology, Soroka Medical Center, Faculty of Health Sciences, Ben-Gurion University of Negev, Beer-Sheva, Israel.
authors.forename: G
authors.initials: G
authors.lastname: Kopernik
authors.forename: E
authors.initials: E
authors.lastname: Avinoach
authors.forename: Y
authors.initials: Y
authors.lastname: Grossman
authors.forename: R
authors.initials: R
authors.lastname: Levy
authors.forename: R
authors.initials: R
authors.lastname: Yulzari
authors.forename: B
authors.initials: B
authors.lastname: Rogachev
authors.forename: A
authors.initials: A
authors.lastname: Douvdevani
mesh_terms: D001202:Ascitic Fluid / Q000166:cytology; D002245:Carbon Dioxide / Q000494:pharmacology*; D002478:Cells, Cultured / Q000187:drug effects; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects / Q000201:enzymology; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism; D009852:Omentum; D010537:Peritoneum / Q000166:cytology / Q000187:drug effects*; D011028:Pneumoperitoneum, Artificial; D013481:Superoxides / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D013481:Superoxides; D002245:Carbon Dioxide