title: Release of chemical mediators and inflammatory cell influx during early allergic reaction in the nose: effect of furosemide.
abstract: BACKGROUND
  We evaluated the effect of furosemide on allergen-induced rhinitis in a double-blind, crossover, placebo-controlled experiment.
  
  
  METHODS
  Fourteen patients with rhinitis who were allergic to house dust were nebulized with an intranasal dose of 20 mg of furosemide or placebo before allergen challenge with an extract of Dermatophagoides pteronyssinus (100 BU). Clinical evaluation and nasal lavages with normal saline solution were performed at baseline; after placebo-furosemide nebulization, and at 10, 30, and 60 minutes after allergen challenge. Number of sneezes and a composite symptom score were recorded to evaluate clinical response. Prostaglandin E2 (PGE2), PGD2 peptide leukotrienes and 15-hydroxy, 5,8,11,13-eicosatetraenoic acid (15-HETE) were measured by radioimmunoassay in nasal lavages. Cells were counted and classified as epithelial cells, neutrophils, eosinophils, and others.
  
  
  RESULTS
  No differences in either clinical symptoms or cell influx after allergen challenge were found between furosemide and placebo groups. PGE2 levels did not change after provocation, and furosemide had no effect on its production. Ten minutes after antigen challenge there was a marked increase of PGD2 (p < 0.01), peptide leukotrienes (p < 0.01), and 15-HETE (not significant) on both study days. However, no significant differences in the release of eicosanoids were found between furosemide and placebo groups.
  
  
  CONCLUSIONS
  Our observations in the nasal mucosa suggest that furosemide has no effect on the release of proinflammatory and bronchoconstrictor metabolites (PGD2, peptide leukotrienes, and 15-HETE). In contrast to bronchial asthma, allergen-induced rhinitis was not effectively prevented by furosemide.
authors.affiliation: Servei de Pneumologia, Hospital Clínic, Facultat de Medicina, Universitat de Barcelona, Spain.
authors.forename: J
authors.initials: J
authors.lastname: Prat
authors.forename: J
authors.initials: J
authors.lastname: Mullol
authors.forename: I
authors.initials: I
authors.lastname: Ramis
authors.forename: J
authors.initials: J
authors.lastname: Roselló-Catafau
authors.forename: A
authors.initials: A
authors.lastname: Xaubet
authors.forename: I
authors.initials: I
authors.lastname: Nerin
authors.forename: E
authors.initials: E
authors.lastname: Gelpí
authors.forename: C
authors.initials: C
authors.lastname: Picado
mesh_terms: D000328:Adult; D016718:Arachidonic Acid / Q000037:antagonists & inhibitors / Q000378:metabolism; D002452:Cell Count / Q000187:drug effects; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use; D004311:Double-Blind Method; D004804:Eosinophils / Q000473:pathology; D005260:Female; D005665:Furosemide / Q000627:therapeutic use*; D006801:Humans; D016859:Lipoxygenase Inhibitors / Q000627:therapeutic use; D008297:Male; D009297:Nasal Mucosa / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D009504:Neutrophils / Q000473:pathology; D012221:Rhinitis, Allergic, Perennial / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology
chemical_list: D016861:Cyclooxygenase Inhibitors; D016859:Lipoxygenase Inhibitors; D016718:Arachidonic Acid; D005665:Furosemide