Failure of acute hypoxia to alter pulmonary prostaglandin metabolism in dogs.
We studied the effects of acute hypoxia (Fi02 = 0.09-0.11, 20 min.) on transpulmonary plasma prostaglandin (PG) concentrations in ten anesthetized, paralyzed, artificially ventilated dogs. Concentrations of 6-keto-PGF1 alpha, TxB2, PGE2, PGF2 alpha, and 13,14-dihydro-15-keto-PGF2 alpha were measured from the pulmonary artery and abdominal aorta using radioimmunoassay. In an additional six dogs, the effects of arachidonic acid (AA) infusions (100 mcg/kg/min) during normoxia and acute hypoxia were determined. Compared to normoxic conditions, acute hypoxia increased pulmonary artery pressure (p less than 0.05), decreased both the arterial oxygen tension (PaO2) and the alveolar-to-arterial oxygen tension gradient (A-aDO2) (p less than 0.05), but did not affect transpulmonary plasma PG concentrations. AA infusions significantly (p less than 0.05) increased 6-keto-PGF1 alpha independent of FiO2. Acute hypoxia failed to elicit a pulmonary pressor response in the AA-treated animals although PaO2 and A-aDO2 decreased (p less than 0.05). 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.
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000818:Animals; D015237:Dinoprost; D015232:Dinoprostone; D004285:Dogs; D005260:Female; D006339:Heart Rate; D000860:Hypoxia / Q000378:metabolism*; D007700:Kinetics; D008168:Lung / Q000502:physiology*; D008297:Male; D011453:Prostaglandins / Q000097:blood / Q000378:metabolism*; D011458:Prostaglandins E / Q000378:metabolism; D011460:Prostaglandins F / Q000378:metabolism; D011652:Pulmonary Circulation
D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D015121:6-Ketoprostaglandin F1 alpha; D015237:Dinoprost; D015232:Dinoprostone