Hypoxia Stimulates Prostacyclin Synthesis by Neonatal Lungs
Hypoxia Stimulates Prostacyclin Synthesis by Neonatal Lungs
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缺氧刺激新生儿肺合成前列环素
DOI：
10.1203/00006450-198409000-00005
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发表时间：
1984
影响因子：
3.6
通讯作者：
C. Leffler
中科院分区：
文献类型：
--
作者：
R. Green;C. Leffler
总结：抑制前列腺素环加氧酶可增强肺缺氧血管收缩。我们使用新生羔羊肺制剂灌注了克雷布斯碳酸氢盐缓冲液，以表征和量化肺血管在缺氧和常氧混合气体通气过程中由内源性花生四烯酸产生的前列腺素。前列腺素（PG） I2合成从正氧通气时的6.4±2.7 ng/min （SEM）增加到缺氧时的14.3±5.4 ng/min，恢复正氧通气后又恢复到4.7±1.2 ng/min。这些数据表明，缺氧刺激新生羔羊肺血管从内源性底物合成前列腺素I2，并提示通过抑制前列腺素环加氧酶增强缺氧肺血管收缩，至少部分是由于干扰了这种血管扩张剂前列腺素的合成。
Summary: Inhibition of prostaglandin cyclooxygenase augments hypoxic pulmonary vasoconstriction. We used a neonatal lamb lung preparation perfused with Krebs' bicarbonate buffer to characterize and quantify prostanoids produced by the pulmonary vasculature from endogenous arachidonic acid in the absence of formed blood elements during ventilation with normoxic and hypoxic gas mixtures. Prostaglandin (PG) I2 synthesis increased from 6.4 ± 2.7 ng/min (SEM) during normoxic ventilation to 14.3 ± 5.4 ng/min during hypoxia and returned to 4.7 ± 1.2 ng/min with resumption of normoxia. These data demonstrate that hypoxia stimulates pulmonary vascular synthesis of prostaglandin I2 from endogenous substrate in neonatal lambs and suggest that the augmentation of hypoxic pulmonary vasoconstriction by prostaglandin cyclooxygenase inhibition is due, at least in part, to interference with the synthesis of this vasodilator prostanoid.