title: Expression of inducible nitric oxide synthase and inflammatory cytokines in alveolar macrophages of ARDS following sepsis.
abstract: OBJECTIVE
  The objective of this study was to evaluate the role of inducible nitric oxide synthase (iNOS) and proinflammatory cytokines in alveolar macrophages (AMs) in the pathogenesis of ARDS following sepsis.
  
  
  METHODS
  ICU in a university hospital.
  
  
  METHODS
  Prospective exploratory, open-labeled study was carried out.
  
  
  METHODS
  A total of 24 patients were investigated: 8 patients diagnosed as having ARDS following sepsis (ARDS group); 8 patients under general anesthesia in the operating room whose lung functions were normal (control group); and 8 patients who were intubated and artificially ventilated for 1 week in the ICU whose lung functions were not deteriorated without fulfilling the ARDS criteria and whose general state fulfilled the sepsis criteria (long-term ventilation group, or LTV group).
  
  
  RESULTS
  The expression of iNOS, interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and interleukin-8 (IL-8) in AMs obtained from BAL fluid (BALF) was determined by the immunofluorescent technique. We observed the significant expression of iNOS, IL-6, and IL-8 only in the ARDS group. Meanwhile, NOx (the sum of NO2- + NO3-) was elevated in the BALF supernatant, and IL-6 and IL-8 levels in both the BALF supernatant and the serum were also elevated in the ARDS group. No significant expressions were detected in the control and the LTV group.
  
  
  CONCLUSIONS
  The result that iNOS was detected only in ARDS patients following sepsis suggests that iNOS together with proinflammatory cytokines produced by AMs might play a pivotal role in the pathogenesis of acute lung injury and be useful for monitoring disorders in the lung in such conditions.
authors.affiliation: Department of Intensive Care and Anesthesiology, Kyoto Prefectural University of Medicine, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Kobayashi
authors.forename: S
authors.initials: S
authors.lastname: Hashimoto
authors.forename: K
authors.initials: K
authors.lastname: Kooguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Kitamura
authors.forename: H
authors.initials: H
authors.lastname: Onodera
authors.forename: Y
authors.initials: Y
authors.lastname: Urata
authors.forename: T
authors.initials: T
authors.lastname: Ashihara
mesh_terms: D000328:Adult; D000368:Aged; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D005260:Female; D005455:Fluorescent Antibody Technique; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D007375:Interleukin-1 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D007378:Interleukins / Q000378:metabolism*; D016676:Macrophages, Alveolar / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II; D011446:Prospective Studies; D011506:Proteins / Q000032:analysis; D011654:Pulmonary Edema / Q000209:etiology / Q000378:metabolism*; D018805:Sepsis / Q000150:complications*
chemical_list: D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D007378:Interleukins; D011506:Proteins; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II