Oxidant- and lipid-induced pulmonary vasoconstriction mediated by arachidonic acid metabolites.
Oxidant- and lipid-induced pulmonary vasoconstriction mediated by arachidonic acid metabolites.
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由花生四烯酸代谢物介导的氧化剂和脂质诱导的肺血管收缩。
DOI：
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发表时间：
1982
期刊：
影响因子：
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通讯作者：
N. Adkinson
中科院分区：
文献类型：
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作者：
G. Gurtner;Philip L. Smith;A. Knoblauch;H. Makhzoumi;R. Traystman;N. Adkinson
在实验中使用离体兔肺灌注Krebs-Henseleit缓冲液在非再循环的方式，我们发现，管理的有机过氧化物，叔丁基过氧化氢（叔丁基-OOH），或Intraperoid，酯化的不饱和脂肪酸的混合物，引起显着的血管加压反应，这是与血栓素水平增加的流出物灌注液。维生素E缺乏动物的肺中对叔丁基-OOH的血管加压反应更大，这可能与这些肺中增加前列环素产生的能力减弱有关。相反，对正常肺给予Intraperoid可导致前列环素显著升高和升压反应较小。升压反应的幅度与血栓素B2与前列环素代谢产物的比率密切相关。这些介质的释放与血管紧张素II引起的肺血管收缩无关。升压反应可被消炎痛完全阻断。我们认为花生四烯酸代谢的环氧化酶途径的激活在氧化性肺损伤的病理生理学中可能是重要的。
In experiments using isolated rabbit lungs perfused with Krebs-Henseleit buffer in a nonrecirculating manner, we found that administration of an organic peroxide, tert-butyl hydroperoxide (t-bu-OOH), or Intralipid, an esterified mixture of unsaturated fatty acids, caused a marked vasopressor response which was associated with increased levels of thromboxane in the effluent perfusate. The vasopressor response to t-bu-OOH was greater in the lungs of vitamin E-deficient animals, and this could be correlated with an attenuated ability to increase prostacyclin production in these lungs. Conversely, administration of Intralipid to normal lungs caused marked increases in prostacyclin and a smaller pressor response. The magnitude of the pressor response was strongly correlated with the ratio of thromboxane B2 to the prostacyclin metabolite. No release of these mediators was associated with pulmonary vasoconstriction caused by administration of angiotensin II. The pressor response could be completely blocked by administration of indomethacin. We propose that this activation of the cyclooxygenase pathway of arachidonic acid metabolism may be important in the pathophysiology of oxidant lung damage.