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Prostaglandin synthetase inhibitors do not decrease hypoxic pulmonary vasoconstriction

E K Weir, I F McMurtry, A Tucker

    Journal of Applied Physiology
    |November 1, 1976
    PubMed
    Summary
    This summary is machine-generated.

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    Prostaglandins do not mediate hypoxic pulmonary vasoconstriction. Instead, hypoxia stimulates prostaglandin synthesis, which causes pulmonary vasodilation, opposing the constrictive effects of hypoxia.

    Area of Science:

    • Cardiovascular Physiology
    • Pulmonary Circulation
    • Vasoactive Mediators

    Background:

    • Prostaglandins are vasoactive substances released during hypoxia or ischemia.
    • A prostaglandin's role in mediating the pulmonary vascular pressor response to alveolar hypoxia has been suggested.

    Purpose of the Study:

    • To investigate the role of prostaglandins in mediating the pulmonary vascular pressor response to alveolar hypoxia.

    Main Methods:

    • Pulmonary pressor responses to hypoxia were measured before and after prostaglandin synthesis inhibition.
    • Inhibition was achieved using meclofenamate in dogs, calves, and isolated rat lungs.
    • Indomethacin was also used in additional dogs to inhibit synthesis.

    Main Results:

    Related Experiment Videos

    • Pulmonary pressor responses to hypoxia were significantly increased, not reduced, after prostaglandin synthesis antagonism.
    • This effect was consistent across species (dogs, calves, rats) and with both antagonists.

    Conclusions:

    • Prostaglandins do not mediate hypoxic pulmonary vasoconstriction.
    • Hypoxic vasoconstriction appears to stimulate prostaglandin synthesis, leading to a net vasodilatory effect that opposes pulmonary constriction.