To determine whether cyclooxygenase products mediated the attenuation of hypoxic pulmonary vasoconstriction induced by estradiol, we measured pulmonary arterial pressure at a flow of 50 ml·min-1·kg-1 (Ppa50) during steady-state exposures to inspired O2 tensions (PIO2) between 0 and 200 Torr in isolated lungs of juvenile ewes. Intramuscular estradiol (10 mg) 44-60 h before study significantly decreased perfusate concentrations of 6-ketoprostaglandin F(1α) (6-keto-PGF(1α)), the stable metabolite of the pulmonary vasodilator, prostacyclin, but did not significantly affect the stimulus-response relationship between PI(O2) and Ppa50. Estradiol (20 mg) 3-5 days before study increased 6-keto-PGF(1α) concentrations and decreased Ppa50 at PI(O2) of 10, 30, and 50 Torr. Indomethacin added to the perfusate of these lungs reduced 6-keto-PGF(1α) to undetectable levels and altered the estradiol-induced attenuation, increasing Ppa50 at PI(O2) of 10 and 30 Torr, but decreasing Ppa50 at PI(O2) of 200 Torr. Despite these effects, Ppa50 remained lower than the values measured in lungs not treated with estradiol. These results suggest that the estradiol-induced attenuation of the hypoxic stimulus-response relationship was mediated only in part by cyclooxygenase products, the net effects of which were vasodilation at PI(O2) of 10 and 30 Torr, but vasoconstriction at PI(O2) of 200 Torr.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of applied physiology|
|State||Published - Dec 1 1986|
ASJC Scopus subject areas
- Physiology (medical)