Failure of acute hypoxia to alter pulmonary prostaglandin metabolism in dogs

Mary A. Moon, Richard J. Lemen, Stuart F. Quan

    Research output: Contribution to journalArticlepeer-review

    5 Scopus citations

    Abstract

    We studied the effects of acute hypoxia (Fi02=0.09-0.11, 20 min,.) on transpulmonary plasma prostaglandin (PG) concentrations in ten anaesthetized, paralyzed, artificially ventilated dogs. Concentrations of 6-keto-PGF1α, TxB2, PGE2, PGF2α, and 13, 13-dihydro-15-keto-PGF2α were measured from the pulmonary artery and abdominal aorta using radioimmunoassay. In an additional six dogs, the effects of arachidonic acid (AA) infusions (100 mg/kg/min) during normoxia and acute hypoxia were determined. Compared to normoxic conditions, acute hypoxia increased pulmonary artery pressure (p<0.0), decreased both the arterial oxygen tension (Pa02) and the alveolar-to-arterial oxygen tension gradient (A-aD02) (p <0.05), but did not affect transpulmonary plasma PG concentrations. AA infusions significantly (p <0.05) increased 6-keto-PGF1α independent of Fi02. Acute hypoxia failed to elicit a pulmonary pressor response in the AA-treated animals although Pa02 and A-aD02 decreased (p<0.5). These data in healthy dogs suggest that (1) acute hypoxia does not alter net pulmonary PG metabolism, (2) prostacyclin synthesis is stimulated by increased plasma AA concentrations and (3) this effect may block normal pressor responses to hypoxic stimuli.

    Original languageEnglish (US)
    Pages (from-to)615-627
    Number of pages13
    JournalProstaglandins
    Volume25
    Issue number5
    DOIs
    StatePublished - May 1983

    ASJC Scopus subject areas

    • Biochemistry
    • Endocrinology

    Fingerprint

    Dive into the research topics of 'Failure of acute hypoxia to alter pulmonary prostaglandin metabolism in dogs'. Together they form a unique fingerprint.

    Cite this