title: Effect of inflammatory mediators on the physiology of the human Fallopian tube.
abstract: The physiological basis for the use of non-steroidal anti-inflammatory drugs (NSAIDs) in the treatment of acute pelvic pain in women was examined in terms of: (i) the electrophysiological responses of epithelial cells in the human Fallopian tube; and (ii) the longitudinal and circular contractions of the myosalpinx. Epithelial cells were grown as a polarized layer in primary culture, and transepithelial potential difference (p.d.) and short-circuit current (I(scc)) were recorded using a modified Ussing chamber. The inflammatory mediators histamine (0.1-100.0 micromol l(-1)) and platelet activating factor (PAF) (1.9-1900.0 nmol l(-1)) increased p.d. and I(scc) in a dose-dependent manner. Pre-incubation with the NSAID diclofenac sodium (100 micromol l(-1)) inhibited the histamine- and PAF-induced stimulation of p.d. and I(scc). Aspirin (100 micromol l(-1)), ibuprofen (100 micromol l(-1)), indomethacin (100 micromol l(-1)) or naproxen (100 micromol l(-1)) were only partially effective. Histamine (0.1-1000.0 micromol l(-1)) increased the frequency of contractions of longitudinal and circular smooth muscle in segments of Fallopian tube in vitro, in a dose-dependent manner. Pre-incubation with diclofenac significantly reduced the histamine-induced stimulation of tubal smooth muscle contraction at the higher doses of histamine. The other NSAIDs had no effect. These data provide evidence that diclofenac downregulates acute inflammation in the human Fallopian tube and may be of use as an anti-inflammatory agent in the treatment of pelvic inflammatory disease.
authors.affiliation: Department of Biology, University of York, PO Box No 373, York YO10 5YW, UK.
authors.forename: Sandra J
authors.initials: SJ
authors.lastname: Downing
authors.forename: Jaqueline I
authors.initials: JI
authors.lastname: Tay
authors.forename: Stephen D
authors.initials: SD
authors.lastname: Maguiness
authors.forename: Alan
authors.initials: A
authors.lastname: Watson
authors.forename: Henry J
authors.initials: HJ
authors.lastname: Leese
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology / Q000627:therapeutic use; D001241:Aspirin / Q000494:pharmacology; D002478:Cells, Cultured; D004008:Diclofenac / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004553:Electric Conductivity; D004594:Electrophysiology; D004847:Epithelial Cells / Q000502:physiology; D005187:Fallopian Tubes / Q000502:physiology*; D005260:Female; D006632:Histamine / Q000494:pharmacology; D006801:Humans; D007052:Ibuprofen / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D018836:Inflammation Mediators / Q000502:physiology*; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects / Q000502:physiology; D009288:Naproxen / Q000494:pharmacology; D017699:Pelvic Pain / Q000188:drug therapy; D010972:Platelet Activating Factor / Q000494:pharmacology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D018836:Inflammation Mediators; D010972:Platelet Activating Factor; D004008:Diclofenac; D009288:Naproxen; D006632:Histamine; D001241:Aspirin; D007052:Ibuprofen; D007213:Indomethacin