Thromboxane rather than platelet activating factor mediates pulmonary vasoconstriction after antigen challenge in rabbits

Keiji Enzan, Shin Kurosawa, Naohumi Yoshioka, Hideo Inaba

    Research output: Contribution to journalArticlepeer-review

    2 Citations (Scopus)

    Abstract

    To investigate whether thromboxane and/or platelet activating factor (PAF) mediate the pulmonary vasoconstrictive response to antigen in vivo, we intra-arterially injected human erythrocytes as antigen into sensitized rabbits after administration of putative inhibitors: a cyclooxygenase synthetase inhibitor (indomethacin, 5 mg·kg-1), a thromboxane synthetase inhibitor (OKY 046, 10 mg·kg-1 + 100 μg·kg-1·min-1), and a PAF blocker (CV6209, .1 mg·kg-1). Pulmonary artery and airway pressures significantly increased after the antigen challenge in sensitized rabbits, but did not in nonsensitized rabbits. Both indomethacin and OKY046 significantly inhibited the increase in pulmonary artery pressure after the antigen challenge, while CV6209 did not. CV6209 significantly attenuated the decrease in femoral artery pressure after the antigen challenge, while neither indomethacin nor OKY046 did. There were no significant differences in the increase in airway pressure among the groups. We conclude that thromboxane rather than PAF mediates the pulmonary vasoconstriction after the antigen challenge and that mediators other than thromboxane and PAF mediate bronchoconstriction after the antigen challenge in sensitized rabbits.

    Original languageEnglish
    Pages (from-to)183-187
    Number of pages5
    JournalShock
    Volume6
    Issue number3
    DOIs
    Publication statusPublished - 1996 Jan 1

    ASJC Scopus subject areas

    • Emergency Medicine
    • Critical Care and Intensive Care Medicine

    Fingerprint Dive into the research topics of 'Thromboxane rather than platelet activating factor mediates pulmonary vasoconstriction after antigen challenge in rabbits'. Together they form a unique fingerprint.

    Cite this