Effects of 100% oxygen on lung vascular function in awake sheep.
Effects of 100% oxygen on lung vascular function in awake sheep.
复制标题
%20of%20100%%20氧气%20对%20肺%20血管%20功能%20对%20清醒%20羊的影响。
DOI：
10.1152/jappl.1983.54.5.1379
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Brigham,KL
中科院分区：
文献类型：
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作者：
Newman,JH;Loyd,JE;English,DK;Ogletree,ML;Fulkerson,WJ;Brigham,KL
本研究的目的是确定成年绵羊持续呼吸100%氧气期间肺毒性的时间过程。准备绵羊用于长期测量血管压、心输出量、气体交换和收集肺淋巴液。气管造口术允许准确输送100%氧气、压缩空气或低氧气体。6只绵羊呼吸100%氧气72-96 h，4只绵羊呼吸压缩空气96 h。除了低氧挑战[吸入O2的分数浓度（FIo 2）= 0.12]，一些绵羊接受前列腺素H2（PGH 2）类似物输注，以进一步评估肺血管反应性。通过改良博伊登室中的粒细胞迁移来测量肺淋巴和血液趋化活性。采用死后肺含水量和光镜检查来测量肺水肿。所有呼吸100%氧气的绵羊在72（n = 2）和96 h（n = 4）之间死亡。绵羊呼吸氧气通过以下测量结果证明了肺毒性：1）富含蛋白质的肺淋巴液流量增加4倍，2）肺泡-动脉Po 2差异增加（大于20 Torr，FIo 2 = 0.21）和高碳酸血症，3）平均血管外肺水/干肺重量为5.7（对照= 3.3），以及间质和肺泡水肿的组织学证据。在吸氧72-96小时内，肺淋巴液的趋化活性在基线时增加了8倍。在绵羊呼吸氧气，缺氧升压反应下降了50%，在48小时，并在72-96小时有一个完全没有缺氧血管收缩。肺淋巴前列环素代谢产物无增加，甲氨蝶呤钠不能恢复升压反应。在绵羊呼吸压缩空气时，肺血管反应性、淋巴流量或趋化活性均未发生上述变化。我们的结论是，长时间呼吸纯氧导致肺水肿，增加肺血管通透性和呼吸衰竭的结果，水肿和肺血管反应性的损失。
The purpose of this study was to define the time course of pulmonary toxicity during continuous breathing of 100% oxygen in adult sheep. Sheep were prepared for chronic measurement of vascular pressures, cardiac output, gas exchange, and for collection of lung lymph. Tracheostomies allowed accurate delivery of either 100% oxygen, compressed air, or hypoxic gas. Six sheep breathed 100% oxygen for 72–96 h, and four sheep breathed compressed air for 96 h. In addition to hypoxic challenges [fractional concentration of inspired O2 (FIo2) = 0.12], some sheep received prostaglandin H2 (PGH2)-analogue infusions to further assess pulmonary vascular reactivity. Lung lymph and blood chemotactic activity were measured by granulocyte migration in modified Boyden chambers. Postmortem lung water content and light microscopy were used to measure pulmonary edema. All sheep breathing 100% oxygen died between 72 (n = 2) and 96 h (n = 4). Sheep breathing oxygen demonstrated lung toxicity by measurements of 1) a fourfold increase in flow of protein-rich lung lymph, 2) increased alveolar-arterial difference in Po2 (greater than 20 Torr on FIo2 = 0.21) and hypercapnic acidemia, and 3) a mean extravascular lung water/dry lung weight of 5.7 (controls = 3.3), and histological evidence of interstitial and alveolar edema. Chemotactic activity in lung lymph at base line increased eightfold within 72–96 h of oxygen breathing. In sheep breathing oxygen, the hypoxic pressor response decreased by 50% at 48 h, and by 72–96 h there was a total absence of hypoxic vasoconstriction. There was no increase in lung lymph prostacyclin metabolite, and sodium meclofenamate did not restore the pressor response. In sheep breathing compressed air none of these changes in pulmonary vascular reactivity, lymph flow, or chemotactic activity occurred. We conclude that prolonged breathing of pure oxygen causes pulmonary edema by increasing lung vascular permeability and that respiratory failure results from both edema and loss of pulmonary vascular reactivity.