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首页> 外文期刊>American Journal of Physiology >Reactive oxygen species mediate arachidonic acid-induced dilation in porcine coronary microvessels.
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Reactive oxygen species mediate arachidonic acid-induced dilation in porcine coronary microvessels.

机译：活性氧介导猪冠状动脉微血管中花生四烯酸诱导的扩张。

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摘要

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 microm 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 O2- scavenger), 250 U/ml PEG-catalase (a H2O2 scavenger), or the cyclooxygenase (COX) inhibitors indomethacin (10 microM) or diclofenac (10 microM) for 30 min. After endothelin constriction (30-60% of resting diameter), cumulative concentrations of AA (10(-10)-10(-5)M) were added and internal diameters measured by video microscopy. AA (10-7 M) 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.
机译：已经提出了活性氧（ROS）介导微循环中的血管舒张。我们调查了ROS在花生四烯酸（AA）诱导冠状动脉微血管扩张中的作用。将猪心外膜冠状小动脉（直径110 +/- 4微米）安装在含氧Krebs缓冲液中的移液器上。将船只与媒介物或1 mM Tiron（非选择性ROS清除剂），250 U / ml聚乙二醇（PEG）-超氧化物歧化酶（SOD; O2-清除剂），250 U / ml PEG-过氧化氢酶（H2O2清除剂）孵育，或环氧合酶（COX）抑制剂消炎痛（10 microM）或双氯芬酸（10 microM）持续30分钟。内皮素收缩（静息直径的30-60％）后，添加累积浓度的AA（10（-10）-10（-5）M），并通过视频显微镜测量内径。 AA（10-7 M）产生37 +/- 6％的扩张，通过消炎痛（4 +/- 7％，P <0.05）或双氯芬酸（-8 +/- 8％，P <0.05）消除），以及Tiron（-4 +/- 5％，P <0.05），PEG-SOD（-10 +/- 6％，P <0.05）或PEG-过氧化氢酶（1 +/- 4％， P <0.05）。小冠状动脉与[3H] AA一起孵育会导致前列腺素的形成，而后者会被消炎痛阻滞。在微血管的单独研究中，AA诱导了浓度敏感的氧化剂敏感性探针二氯二氢荧光素二乙酸酯的荧光增加，这被吲哚美辛或SOD +过氧化氢酶预处理所抑制。我们得出的结论是，在猪冠状动脉微血管中，COX衍生的ROS有助于AA诱导的血管舒张。

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