Reactive oxygen species mediate arachidonic acid-induced dilation in porcine coronary microvessels.
Reactive oxygen species mediate arachidonic acid-induced dilation in porcine coronary microvessels.
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活性氧介导花生四烯酸诱导的猪冠状微血管扩张。
DOI：
10.1152/ajpheart.00456.2003
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Dellsperger,KevinC
中科院分区：
文献类型：
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作者：
Oltman,ChristineL;Kane,NealL;MillerJr,FrancisJ;Spector,ArthurA;Weintraub,NealL;Dellsperger,KevinC
活性氧簇(ROS)被认为可以调节微循环中的血管扩张。我们研究了ROS在花生四烯酸(AA)诱导的冠状动脉微血管扩张中的作用。将直径为(110±4)μm的猪心外膜冠状小动脉固定在充氧Krebs缓冲液中的吸管上。血管与赋形剂或1 mM TIron(非选择性ROS清除剂)、250U/ml的聚乙二醇化超氧化物歧化酶(SOD)孵育；[fleqn，10pt，LegalPaper]{文章}\usepackage{amssymb}\usepackage{amsfonts}\usepackage{amsath}\Page Style{Empty}\Begin{Document}(\mathm{O}_{2}^{-}\)\end{Document}清道夫)、250U/ml聚乙二醇过氧化氢酶(H_2O_2清除剂)或环氧合酶(COX)抑制剂消炎痛(10μM)或双氯芬酸(10μM)30分钟。血管内皮缩窄后(静息直径的30-60%)，加入累积浓度的AA(10-10-10-5M)，在视频显微镜下测量内径。AA(10-7M)产生37±6%的扩张率，可被消炎痛(4±7%，P<0.05)或双氯芬酸(-8±8%，P<0.05)、TIron(-4±5%，P<0.05)、聚乙二醇超氧化物歧化酶(-10±6%，P<0.05)或聚乙二醇过氧化氢酶(1±4%，P<0.05)所消除。小冠状动脉与[~3H]AA孵育可产生前列腺素，该作用可被吲哚美辛阻断。在单独的微血管研究中，AA诱导氧化剂敏感的探针二氯二氢荧光素二乙酸酯的荧光浓度依赖地增加，该作用可被消炎痛或超氧化物歧化酶+过氧化氢酶抑制。我们认为，在猪冠状动脉微血管中，COX衍生的ROS参与了AA诱导的血管扩张。
Reactive oxygen species (ROS) have been proposed to mediate vasodilation in the microcirculation. We investigated the role of ROS in arachidonic acid (AA)-induced coronary microvascular dilation. Porcine epicardial coronary arterioles (110 ± 4 μm diameter) were mounted onto pipettes in oxygenated Krebs buffer. Vessels were incubated with vehicle or 1 mM Tiron (a nonselective ROS scavenger), 250 U/ml polyethylene-glycolated (PEG)-superoxide dismutase (SOD; an \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{O}_{2}^{-}\) \end{document} scavenger), 250 U/ml PEG-catalase (a H2O2scavenger), or the cyclooxygenase (COX) inhibitors indomethacin (10 μM) or diclofenac (10 μM) for 30 min. After endothelin constriction (30–60% of resting diameter), cumulative concentrations of AA (10–10–10–5M) were added and internal diameters measured by video microscopy. AA (10–7M) produced 37 ± 6% dilation, which was eliminated by the administration of indomethacin (4 ± 7%,P< 0.05) or diclofenac (–8 ± 8%,P< 0.05), as well as by Tiron (–4 ± 5%,P< 0.05), PEG-SOD (–10 ± 6%,P< 0.05), or PEG-catalase (1 ± 4%,P< 0.05). Incubation of small coronary arteries with [3H]AA resulted in the formation of prostaglandins, which was blocked by indomethacin. In separate studies in microvessels, AA induced concentration-dependent increases in fluorescence of the oxidant-sensitive probe dichlorodihydrofluorescein diacetate, which was inhibited by pretreatment with indomethacin or by SOD + catalase. We conclude that in porcine coronary microvessels, COX-derived ROS contribute to AA-induced vasodilation.