title: Carbon dioxide pneumoperitoneum alters acute-phase response induced by lipopolysaccharide.
abstract: BACKGROUND
  As laparoscopic surgery continues to expand in scope, septic patients will be exposed to carbon dioxide (CO2) pneumoperitoneum in increasing numbers. The biologic advantages or disadvantages of laparoscopic surgery in the setting of sepsis/inflammation are not known. In a rat model, we investigated whether CO2 pneumoperitoneum alters the inflammatory response induced by bacterial lipopolysaccharide (LPS).
  
  
  METHODS
  Male rats were injected via the penile vein with LPS (1 mg/kg). Five hours later, the animals (n = 5) were subjected to CO2 pneumoperitoneum (group I) for 1h; the animals of group II (n = 5) served as controls (no pneumoperitoneum). At 6 h, all animals were killed and the liver harvested for analysis of hepatic acute-phase gene expression. Total RNA was isolated and analyzed by Northern blot hybridization with probes for alpha-2 macroglobulin (A2M) and detected by autoradiography. The film in the linear range of exposure was quantitated using an imaging system. The signal intensity corresponding to A2M mRNA was normalized by the signal corresponding to 28S rRNA detected by staining with methylene blue.
  
  
  RESULTS
  The mRNA levels in group II was 6.5 +/- 0.9 vs 2.8 +/- 0.4 in group I. As compared with rats that received LPS only, those that received a combination of LPS and CO2 showed a reduction in A2M mRNA levels (57.4%, p = 0.006).
  
  
  CONCLUSIONS
  These data demonstrate that the presence of CO2 pneumoperitoneum reduces the inflammatory response established by LPS. This finding challenges the generally accepted notion that smaller incisions alone account for the observed benefits of laparoscopic surgery. It further suggests that CO2 pneumoperitoneum - aided laparoscopic surgery impedes the inflammatory response and may therefore offer specific benefits over conventional surgery.
authors.affiliation: Department of Surgery, The Johns Hopkins Medical Institutions, Blalock 665, 600 North Wolfe Street, Baltimore, MD 21205, USA.
authors.forename: C
authors.initials: C
authors.lastname: Are
authors.forename: M A
authors.initials: MA
authors.lastname: Talamini
authors.forename: K
authors.initials: K
authors.lastname: Murata
authors.forename: A
authors.initials: A
authors.lastname: De Maio
mesh_terms: D000210:Acute-Phase Reaction / Q000139:chemically induced* / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D001345:Autoradiography / Q000379:methods; D015152:Blotting, Northern / Q000379:methods; D002245:Carbon Dioxide / Q000009:adverse effects* / Q000627:therapeutic use; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics; D007275:Injections, Intravenous; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000494:pharmacology*; D008099:Liver / Q000737:chemistry / Q000378:metabolism; D008297:Male; D010413:Penis / Q000098:blood supply; D011028:Pneumoperitoneum, Artificial / Q000009:adverse effects*; D012313:RNA / Q000235:genetics; D015347:RNA Probes / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D000511:alpha-Macroglobulins / Q000235:genetics
chemical_list: D008070:Lipopolysaccharides; D015347:RNA Probes; D000511:alpha-Macroglobulins; D002245:Carbon Dioxide; D012313:RNA