title: Nonsteroidal anti-inflammatory drugs alter the human mesothelial pleural permeability via ion cellular transportation by inhibiting prostaglandin synthesis.
abstract: BACKGROUND
  Nonsteroidal anti-inflammatory drugs (NSAIDs) are used in clinical practice as analgesics or anti-inflammatory drugs. Studies have implicated them in participating in permeability throughout various tissues such as the kidneys and lungs.
  
  
  OBJECTIVE
  The effect of NSAIDs on the pleural permeability and the underlying mechanisms whereby this effect is mediated were investigated.
  
  
  METHODS
  Parietal pleural specimens were obtained from patients subjected to thoracic surgery and were mounted in Ussing chambers. Solutions containing paracetamol, acetylsalicylic acid, diclofenac, lornoxicam, parecoxib and ibuprofen were added in the chambers facing the pleural and the outer-pleural surface. Prostaglandin E(2) was similarly used to investigate prostaglandin synthesis involvement at low and high doses. Amiloride- and ouabain-pretreated specimens were used in order to investigate ion transportation involvement. Transmesothelial resistance (R(TM)) was determined as a permeability indicator.
  
  
  RESULTS
  Paracetamol, acetylsalicylic acid, diclofenac, lornoxicam and ibuprofen increased R(TM) on the pleural and outer-pleural surface, inhibited by amiloride and ouabain. Parecoxib had no effect on the R(TM). Prostaglandin decreased R(TM) on the pleural and outer-pleural surface inhibited by amiloride, ouabain and ibuprofen.
  
  
  CONCLUSIONS
  NSAIDs, except parecoxib, induce a rapid decrease of the pleural permeability by inhibiting cellular transportation, an effect that is mediated by prostaglandin synthesis inhibition.
authors.affiliation: Department of Thoracic and Vascular Surgery, Evangelismos Hospital, Athens, Greece. kouritas@otenet.gr
authors.forename: Vasileios K
authors.initials: VK
authors.lastname: Kouritas
authors.forename: Charalambos
authors.initials: C
authors.lastname: Zisis
authors.forename: Ion
authors.initials: I
authors.lastname: Bellenis
authors.forename: Konstantinos I
authors.initials: KI
authors.lastname: Gourgoulianis
authors.forename: Paschalis A
authors.initials: PA
authors.lastname: Molyvdas
authors.forename: Chrisi
authors.initials: C
authors.lastname: Hatzoglou
mesh_terms: D000584:Amiloride / Q000494:pharmacology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D015232:Dinoprostone / Q000378:metabolism*; D017097:Electric Impedance; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004848:Epithelium / Q000187:drug effects; D006801:Humans; D066298:In Vitro Techniques; D017136:Ion Transport / Q000187:drug effects*; D010042:Ouabain / Q000494:pharmacology; D010539:Permeability / Q000187:drug effects*; D010994:Pleura / Q000187:drug effects* / Q000378:metabolism; D026941:Sodium Channel Blockers / Q000494:pharmacology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D004791:Enzyme Inhibitors; D026941:Sodium Channel Blockers; D010042:Ouabain; D000584:Amiloride; D015232:Dinoprostone