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11,12-EET 增加门脉血流阻力，并可能在门静脉高压症的内皮功能障碍中发挥作用。

11,12-EET increases porto-sinusoidal resistance and may play a role in endothelial dysfunction of portal hypertension.

机构信息

Department of Clinical and Experimental Medicine, University of Padova, Via Giustiniani 2, 35100 Padova, Italy.

出版信息

Prostaglandins Other Lipid Mediat. 2011 Nov;96(1-4):72-5. doi: 10.1016/j.prostaglandins.2011.08.002. Epub 2011 Aug 11.

DOI:10.1016/j.prostaglandins.2011.08.002
PMID:21856435
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4540347/
Abstract

CYP450-dependent epoxyeicosatrienoic acids (EETs) are potent arterial vasodilators, while 20-hydroxyeicosatatraenoic acid (20-HETE) is a vasoconstrictor. We evaluated their role in the control of portal circulation in normal and cirrhotic (CCl(4) induced) isolated perfused rat liver. Phenylephrine (PE) and endothelin-1 (ET-1) increased portal perfusion pressure, as did arachidonic acid (AA), 20-HETE, and 11,12-EET. Inhibition of 20-HETE with 12,12-dibromododecenoic acid (DBDD) did not affect basal pressure nor the responses to PE, ET-1, or AA. However, inhibition of epoxygenase with miconazole caused a significant reduction in the response to ET-1 and to AA, without affecting neither basal pressure nor the response to PE. Hepatic vein EETs concentration increased in response to ET-1, and was increased in cirrhotic, compared to control, livers. 20HETE levels were non-measurable. Miconazole decreased portal perfusion pressure in cirrhotic livers. In conclusion, 20HETE and EETs increase portal resistance; EETs, but not 20-HETE, mediate in part the pressure response to ET-1 in the portal circulation and may be involved in pathophysiology of portal hypertension.

摘要

CYP450 依赖性环氧二十碳三烯酸 (EETs) 是强效的动脉血管舒张剂，而 20-羟二十碳四烯酸 (20-HETE) 则是血管收缩剂。我们评估了它们在正常和肝硬化（CCl4 诱导）离体灌注大鼠肝中对门脉循环控制的作用。苯肾上腺素 (PE) 和内皮素-1 (ET-1) 增加门脉灌注压，花生四烯酸 (AA)、20-HETE 和 11,12-EET 也是如此。用 12,12-二溴十二烯酸 (DBDD) 抑制 20-HETE 并不影响基础压力或对 PE、ET-1 或 AA 的反应。然而，用咪康唑抑制环氧合酶会导致对 ET-1 和 AA 的反应显著减少，而对基础压力或 PE 的反应没有影响。肝静脉 EETs 浓度在 ET-1 反应中增加，并且在肝硬化中比在对照组中增加。20-HETE 水平不可测量。咪康唑降低了肝硬化肝脏的门脉灌注压。总之，20-HETE 和 EETs 增加门脉阻力；EETs，但不是 20-HETE，部分介导了 ET-1 在门脉循环中的压力反应，可能参与了门脉高压的病理生理学。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83fc/4540347/4fa1b3683d93/nihms715239f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83fc/4540347/df1a3122a5eb/nihms715239f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83fc/4540347/a8de76171580/nihms715239f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83fc/4540347/c6a8582975eb/nihms715239f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83fc/4540347/d97cf09c9703/nihms715239f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83fc/4540347/4fa1b3683d93/nihms715239f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83fc/4540347/df1a3122a5eb/nihms715239f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83fc/4540347/a8de76171580/nihms715239f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83fc/4540347/c6a8582975eb/nihms715239f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83fc/4540347/d97cf09c9703/nihms715239f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83fc/4540347/4fa1b3683d93/nihms715239f5.jpg

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