Prostaglandins and estradiol-induced attenuation of hypoxic pulmonary vasoconstriction.
Pretreatment with estradiol (20 mg IM) attenuated vasoreactivity to decreases in inspired PIO2, lowered baseline resistance measured under conditions of maximal vasodilation (PIO2 = 0 mm Hg), and appeared to increase prostaglandin release in isolated, blood-perfused lungs of juvenile female sheep. Indomethacin (40 micrograms/ml) inhibited prostaglandin release and restored hypoxic vasoreactivity in estrogen-treated lungs, but did not alter the estrogen-induced decrease in baseline resistance. These results suggest that estradiol enhanced the production of prostaglandins which secondarily attenuated hypoxic vasoreactivity. The estradiol-induced decrease in baseline resistance, however, must have been mediated by some other mechanism.
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism*; D000818:Animals; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D000860:Hypoxia / Q000378:metabolism*; D008171:Lung Diseases / Q000378:metabolism*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism; D010100:Oxygen / Q000502:physiology; D012119:Respiration; D012756:Sheep; D013929:Thromboxane B2 / Q000378:metabolism; D014661:Vasoconstriction / Q000187:drug effects*
D004958:Estradiol; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D010100:Oxygen