title: Immediate peritoneal response to bacterial contamination during laparoscopic surgery.
abstract: BACKGROUND
  Several studies have shown that laparoscopic surgery (LS) minimizes surgical trauma and the immune function is better preserved. Another major advantage of LS is the lower incidence of septic complications. However, several in vitro studies have shown that CO(2) severely impairs macrophage physiology. In theory, this would reduce the ability to respond to peritoneal contamination. However, there is some controversy in view of the evidence of a better preserved peritoneal response to sepsis. This study analyzed the early response of the peritoneum to contamination in a CO(2) ambience.
  
  
  METHODS
  A total of 192 CD-1 mice were distributed in three groups: group 1, laparotomy (LAP, n = 64); group 2, CO(2) laparoscopy (CO(2)-LC, n = 64); and group 3, wall lift laparoscopy (WL-LC, n = 64). Mice in each group were randomized to receive 1 ml of Escherichia coli suspension (1 x 10(4) colony-forming units/ml) or saline. Peritoneal fluid was obtained at 1.5, 3, 6, and 12 h after surgery. Monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6), and prostaglandin E(2) (PGE(2)) were measured.
  
  
  RESULTS
  MCP-1 levels were significantly greater and higher earlier in group 2 (CO(2)-LC) than in group 1 (LAP) (p < 0.007). Simultaneously, the increment in the traction group (WL-LC, group 3) was significantly higher (p < 0.002) than after laparotomy, with no differences in group 2 (CO(2)-LC). When a contamination was added to the laparotomy subgroup, there was a significant increase compared to the group without contamination (p < 0.5). MCP-1 modifications after contamination in the LAP group were statistically significant and appeared later than in the WL-LC (p < 0.002) and CO(2)-LC groups (p < 0.02). For IL-6, the three models presented a significant increase in the noncontaminated groups. This occurred significantly later in the LAP group. Simultaneously, the increase in IL-6 occurred earlier and was significantly higher in the WL-LC group compared to the LAP group (p < 0.003), without differences between CO(2)-LC and wall lift groups. Significant differences between contaminated and noncontaminated subgroups were only observed in the LC-CO(2) groups. When contaminated, the traction model sustained a higher and earlier rise in IL-6 levels compared to the LAP and LC-CO(2) groups (p < 0.001). For PGE(2), The three models showed a significant increase in PGE(2) levels in the noncontaminated groups. However, there were no significant differences between them. In the contaminated groups, there was no statistical difference between the groups.
  
  
  CONCLUSIONS
  Despite a transient impairment of the immediate peritoneal response to a septic challenge, the degree of injury with LS is lower than that with open surgery, and abdominal infection can therefore be better controlled.
authors.affiliation: Service of Surgery, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain. etargarona@lsp.santpau.es
authors.forename: E M
authors.initials: EM
authors.lastname: Targarona
authors.forename: M
authors.initials: M
authors.lastname: Rodríguez
authors.forename: M
authors.initials: M
authors.lastname: Camacho
authors.forename: C
authors.initials: C
authors.lastname: Balagué
authors.forename: I
authors.initials: I
authors.lastname: Gich
authors.forename: L
authors.initials: L
authors.lastname: Vila
authors.forename: M
authors.initials: M
authors.lastname: Trias
mesh_terms: D000005:Abdomen / Q000601:surgery*; D000818:Animals; D001202:Ascitic Fluid / Q000378:metabolism; D002245:Carbon Dioxide; D018932:Chemokine CCL2 / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D004927:Escherichia coli Infections / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism; D010535:Laparoscopy / Q000009:adverse effects*; D007813:Laparotomy / Q000009:adverse effects; D051379:Mice; D008815:Mice, Inbred Strains; D010537:Peritoneum / Q000378:metabolism*; D011028:Pneumoperitoneum, Artificial; D013530:Surgical Wound Infection / Q000378:metabolism*; D013997:Time Factors
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D015850:Interleukin-6; D002245:Carbon Dioxide; D015232:Dinoprostone