title: Effect of inflammatory mediators on nasal mucosa.
abstract: A technique used for study of permeability and vasodilation in the middle ear has been adapted to study the response of nasal mucosa to common inflammatory mediators involved in the natural production of allergic or infectious rhinitis. All of the mediators tested (histamine, prostaglandin E1, bradykinin, the C3a fraction of complement, Escherichia coli endotoxin, and lysozyme) were found to increase nasal permeability to the isotopic tracer 99mTc as the pertechnetate ion. Histamine increased the permeability of nasal mucosa to technetium-labeled plasma protein. Results indicate that the nasal mucosa is approximately ten times as permeable to the pertechnetate ion as middle ear mucosa. Nasal mucosa was also noted to be permeable to protein, even in the absence of inflammatory mediator, in contrast to prior studies of middle ear mucosa that showed little or no permeability in the absence of inflammatory mediator. In almost all cases, a corresponding change in vasodilation accompanied permeability changes.
mesh_terms: D000818:Animals; D001798:Blood Proteins / Q000378:metabolism; D001920:Bradykinin / Q000494:pharmacology*; D003176:Complement C3; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004731:Endotoxins / Q000494:pharmacology*; D004926:Escherichia coli; D006632:Histamine / Q000494:pharmacology*; D009113:Muramidase / Q000494:pharmacology*; D009297:Nasal Mucosa / Q000187:drug effects*; D010539:Permeability; D011458:Prostaglandins E / Q000494:pharmacology*; D013618:Tachyphylaxis; D014666:Vasomotor System / Q000187:drug effects*
chemical_list: D001798:Blood Proteins; D003176:Complement C3; D004731:Endotoxins; D011458:Prostaglandins E; D006632:Histamine; D009113:Muramidase; D001920:Bradykinin