Sventek J C, Zambraski E J
Aviat Space Environ Med. 1985 Oct;56(10):972-5.
Hyperoxia has been shown to disrupt certain membrane bound enzyme systems within the pulmonary endothelium which are responsible for the metabolism of several endogenous vasoactive compounds. This study was to evaluate whether the potential disruption of the prostaglandin dehydrogenase/reductase and angiotensin converting enzymes, as a consequence of hyperoxia, would alter the activation/deactivation of prostaglandins or the angiotensins (I and II) and thereby alter their peripheral cardiovascular actions. Two groups of anesthetized dogs, one group ventilated with ambient air and the other with 100% oxygen, were given bolus injections of angiotensin I, angiotensin II, prostaglandin E2, sodium nitroprusside, and phenylephrine before and during 8 h of exposure to air or oxygen. The hyperoxic animals demonstrated a significant increase in mean arterial pressure responsiveness to both angiotensin I and angiotensin II. The responsiveness to the drugs increased by 41% for angiotensin I and 43% for angiotensin II. The ambient air control dogs showed no significant changes for any compounds tested. These data indicate that with 8 h of hyperoxia the renin-angiotensin system's ability to influence cardiovascular function is augmented, whereas, the hemodynamic effects of prostaglandins are unaltered.
高氧已被证明会破坏肺内皮细胞内某些膜结合酶系统，这些酶系统负责几种内源性血管活性化合物的代谢。本研究旨在评估高氧导致的前列腺素脱氢酶/还原酶和血管紧张素转换酶的潜在破坏是否会改变前列腺素或血管紧张素（I和II）的激活/失活，从而改变它们的外周心血管作用。两组麻醉犬，一组用空气通气，另一组用100%氧气通气，在暴露于空气或氧气8小时之前和期间，分别静脉注射血管紧张素I、血管紧张素II、前列腺素E2、硝普钠和去氧肾上腺素。高氧动物对血管紧张素I和血管紧张素II的平均动脉压反应性显著增加。血管紧张素I的药物反应性增加了41%，血管紧张素II增加了43%。空气对照犬对所测试的任何化合物均无显著变化。这些数据表明，高氧8小时后，肾素-血管紧张素系统影响心血管功能的能力增强，而前列腺素的血流动力学效应未改变。
