Prostaglandin I2 supports blood flow to hypoxic alveoli in anesthetized dogs.
Prostaglandin I2 supports blood flow to hypoxic alveoli in anesthetized dogs.
复制标题
前列腺素 I2 支持血液流向麻醉犬缺氧的肺泡。
DOI：
10.1152/jappl.1984.56.5.1246
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Lonigro,AJ
中科院分区：
文献类型：
--
作者：
Sprague,RS;Stephenson,AH;Lonigro,AJ
在单侧肺泡缺氧的动物模型中，环加氧酶活性的抑制、免疫反应性6-酮前列腺素F1 α（6-酮- pgf1 α）的估计和前列腺素I2 （PGI2）的给药被用来评估内源性PGI2对抗缺氧肺血管收缩的假设，从而产生血流向缺氧肺泡的重新分配和全身PO2的减少。麻醉犬一只肺100% N2通气，另一只肺100% O2通气。热稀释与电磁流量测量相结合，可以估计每个肺的血流量。吲哚美辛或甲氯芬酸降低n2通气肺流量（P < 0.05），增加全身PO2 （P < 0.05）。同时，主动脉免疫反应性6-酮- pgf1 α浓度下降63 +/- 8% （P < 0.001）。在环氧化酶抑制后，PGI2的增加剂量（0.01、0.025和0.10微克X kg-1 X min-1）增加了n2通气肺的流量，降低了全身PO2 (P < 0.001)，而不影响混合静脉PO2。这些结果表明，由于静脉混合物的增加，系统PO2降低。我们得出结论，PGI2减轻缺氧血管收缩，使血流维持到缺氧肺泡，导致全身PO2降低。
In an animal model of unilateral alveolar hypoxia, inhibition of cyclooxygenase activity, estimates of immunoreactive 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), and administration of prostaglandin I2 (PGI2) were used to evaluate the hypothesis that endogenous PGI2 opposes hypoxic pulmonary vasoconstriction, thereby producing redistribution of blood flow to hypoxic alveoli and reductions in systemic PO2. In anesthetized dogs, one lung was ventilated with 100% N2 and the other with 100% O2. Thermal dilution coupled with electromagnetic flow measurements permitted estimates of blood flow to each lung. Indomethacin or meclofenamate reduced flow to the N2-ventilated lungs (P less than 0.05) and increased systemic PO2 (P less than 0.05). Simultaneously, aortic concentrations of immunoreactive 6-keto-PGF1 alpha decreased 63 +/- 8% (P less than 0.001). Following cyclooxygenase inhibition, incremental doses of PGI2 (0.01, 0.025, and 0.10 micrograms X kg-1 X min-1) increased flow to the N2-ventilated lungs and reduced systemic PO2 (P less than 0.001) without affecting mixed venous PO2. These results suggest that systemic PO2 was reduced because of increased venous admixture. We conclude that PGI2 attenuates hypoxic vasoconstriction which allows flow to be maintained to hypoxic alveoli, resulting in reduced systemic PO2.