Sylvester J T, Gordon J B, Malamet R L, Wetzel R C
Chest. 1985 Oct;88(4 Suppl):252S-254S. doi: 10.1378/chest.88.4_supplement.252s.
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.
用雌二醇(20毫克,肌肉注射)进行预处理可减弱对吸入氧分压降低的血管反应性,降低在最大血管舒张状态(吸入氧分压 = 0毫米汞柱)下测得的基线阻力,并且似乎能增加幼年雌性绵羊离体血液灌注肺中的前列腺素释放。吲哚美辛(40微克/毫升)抑制前列腺素释放并恢复雌激素处理过的肺中的低氧血管反应性,但并未改变雌激素诱导的基线阻力降低。这些结果表明,雌二醇增强了前列腺素的产生,继而减弱了低氧血管反应性。然而,雌二醇诱导的基线阻力降低必定是由其他某种机制介导的。