首页> 外文期刊>Endothelium: Journal of endothelial cell research >Nitric oxide generation by NO donors is enhanced following balloon injury in the porcine coronary artery.
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Nitric oxide generation by NO donors is enhanced following balloon injury in the porcine coronary artery.

机译:猪冠状动脉球囊损伤后,NO供体产生一氧化氮的能力增强。

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摘要

Vasospasm is a complication of cardiological procedures such as balloon angioplasty and may be related to vascular oxidant stress. Although nitric oxide donor drugs are often administered to prevent vasospasm, the response to these drugs in balloon-injured arteries has not been studied. Pig coronary arteries were balloon-injured in vitro and relaxations to nitric oxide (NO)-donating and NO-independent vasodilators studied. Generation of superoxide in response to injury was assayed using dihydroethidium. NO formation on addition of the NO donor drugs was studied using an amperometric sensor. Expression of nitrotyrosine, a peroxynitrite marker, was probed using immunocytochemistry. In vitro injury enhanced sensitivity to the NO donors SNAP and SpermineNONOate but blunted the response to isoprenaline or chromakalim. With both donors, NO formation was significantly enhanced in the presence of an injured vessel. Vascular superoxide generation was also increased throughout the vessel wall and a small increase in nitrotyrosine was detected in the injured vessel media following addition of SNAP. In conclusion, injured vessels were more sensitive to NO donors and this appears to be due to enhanced NO generation by the donor molecule. Increased formation of peroxynitrite within the injured vessel may contribute to the enhanced relaxation in injured vessels.
机译:血管痉挛是心脏病程序(如球囊血管成形术)的并发症,可能与血管氧化应激有关。尽管通常使用一氧化氮供体药物来预防血管痉挛,但尚未研究球囊损伤动脉中对这些药物的反应。体外对猪冠状动脉进行了球囊损伤,并研究了捐赠一氧化氮(NO)和不依赖于NO的血管舒张剂的舒张性。使用二氢乙啶分析了响应于损伤的超氧化物的产生。使用安培传感器研究了添加NO供体药物后NO的形成。使用免疫细胞化学检测过氧亚硝酸盐标记物硝基酪氨酸的表达。体外损伤增强了对NO供体SNAP和SpermineNONOate的敏感性,但减弱了对异丙肾上腺素或chromakalim的反应。对于这两个供体,在受伤血管的存在下,NO的形成均显着增强。添加SNAP后,受损血管中的血管超氧化物生成也增加了整个血管壁,硝基酪氨酸也有少量增加。总之,受伤的血管对NO供体更敏感,这似乎是由于供体分子NO生成增强所致。受伤血管内过氧亚硝酸盐形成的增加可能有助于受伤血管内松弛的增强。

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