title: Role of steroid administration to reduce inflammation after thoracotomy in a rat surgical stress model.
abstract: BACKGROUND
  Unilateral lung surgical insult can lead to bilateral pulmonary inflammation after transthoracic esophagectomy for esophageal cancer. An inflammatory response of the cytokine network induced by surgical stress followed by neutrophil sequestration is the major mechanism involved in these complications. We examined modulation of the inflammatory cytokine and neutrophil sequestration by preoperative steroid administration in a rat thoracotomy model.
  
  
  METHODS
  Adult male rats were subjected to right thoracotomy with pulmonary compression in the surgical stress model. In the another surgical stress model, 10 mg/kg of methylprednisolone (MP) was administered 1 h before the operation intraperitoneally, and peri-operative biological effects of steroid administration to neutrophil sequestration and cytokine-induced neutrophil chemoattractant (CINC) as an inflammatory cytokine were examined. Sham-operated animals were subjected to intubation only.
  
  
  RESULTS
  Surgical insult to the unilateral lung increased local CINC concentration followed by an increase in neutrophil sequestration, wet-to-dry weight ratio in bilateral lungs and systemic CINC concentration. Pre-treatment with methylprednisolone reduced CINC concentration as well as neutrophil sequestration and wet-to-dry weight ratio of both lungs.
  
  
  CONCLUSIONS
  These data suggest that inflammatory changes induced by the unilateral operative procedure occur in both lungs through local inflammatory response. Pre-operative methylprednisolone administration down-regulates cytokine release and neutrophil sequestration, preventing lung edema, and possibly may act as a prophylactic treatment against acute lung injury caused by a so-called "second attack" theory.
authors.affiliation: Department of Surgery, School of Medicine, Keio University, Shinjuku-ku, Tokyo, Japan.
authors.forename: Eiichi
authors.initials: E
authors.lastname: Nakamura
authors.forename: Yuko
authors.initials: Y
authors.lastname: Kitagawa
authors.forename: Soji
authors.initials: S
authors.lastname: Ozawa
authors.forename: Koichi
authors.initials: K
authors.lastname: Suda
authors.forename: Nobutoshi
authors.initials: N
authors.lastname: Ando
authors.forename: Masakazu
authors.initials: M
authors.lastname: Ueda
authors.forename: Masaki
authors.initials: M
authors.lastname: Kitajima
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D054360:Chemokine CXCL1; D019743:Chemokines, CXC / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D015536:Down-Regulation / Q000187:drug effects*; D004797:Enzyme-Linked Immunosorbent Assay; D007249:Inflammation / Q000188:drug therapy* / Q000209:etiology; D008297:Male; D008775:Methylprednisolone / Q000494:pharmacology / Q000627:therapeutic use*; D009504:Neutrophils / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013908:Thoracotomy / Q000009:adverse effects*
chemical_list: D000893:Anti-Inflammatory Agents; D054360:Chemokine CXCL1; D019743:Chemokines, CXC; C513297:Cxcl1 protein, rat; D016207:Cytokines; D008775:Methylprednisolone