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<sub>2</sub> 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<sub>TM</sub>) was determined as a permeability indicator. Results: Paracetamol, acetylsalicylic acid, diclofenac, lornoxicam and ibuprofen increased R<sub>TM</sub> on the pleural and outer-pleural surface, inhibited by amiloride and ouabain. Parecoxib had no effect on the R<sub>TM</sub>. Prostaglandin decreased R<sub>TM</sub> on the pleural and outer-pleural surface inhibited by amiloride, ouabain and ibuprofen. Conclusion: NSAIDs, except parecoxib, induce a rapid decrease of the pleural permeability by inhibiting cellular transportation, an effect that is mediated by prostaglandin synthesis inhibition.
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