Impairment of endothelium-dependent relaxation of rabbit aortas by cigarette smoke extract - Role of free radicals and attenuation by captopril
Impairment of endothelium-dependent relaxation of rabbit aortas by cigarette smoke extract - Role of free radicals and attenuation by captopril
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DOI：
10.1016/s0021-9150(97)06106-6
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发表时间：
1997-06-01
期刊：
影响因子：
5.3
通讯作者：
Yasue, H
中科院分区：
文献类型：
--
作者：
Ota, Y;Kugiyama, K;Yasue, H
研究香烟烟雾提取物（CSE）水溶性成分对离体兔血管内皮依赖性舒张（EDR）的影响。发现与CSE孵育以剂量依赖性方式抑制EDR。用超氧化物歧化酶（SOD）、N-乙酰半胱氨酸、谷胱甘肽或二甲基亚砜（DMSO）等自由基清除剂孵育主动脉条，可减弱CSE对动脉舒张的抑制作用。与卡托普利（3 mM），血管紧张素转换酶抑制剂，共孵育的条，也衰减CSE诱导的血管舒张功能障碍。在使用培养的人内皮细胞的平行实验中，CSE抑制了NOx（一氧化氮（NO）的稳定代谢物）的内皮释放。SOD、DMSO和Captopril可减轻CSE对NO生成的抑制作用，并能减少CSE溶液中的自由基、超氧阴离子和羟自由基。培养的内皮细胞与CSE孵育后，既没有乳酸脱氢酶的释放，也没有台盼蓝排斥试验估计的细胞死亡。结果表明，CSE中的自由基可引起EDR损伤，其机制可能与抑制NO的产生有关，而与CSE的非特异性细胞毒性无关。卡托普利部分通过清除自由基减轻CSE诱导的内皮功能障碍。(C)1997 Elsevier Science爱尔兰有限公司
The aim of this study was to examine the effects of the water soluble component of cigarette smoke extract (CSE) on endothelium-dependent relaxation (EDR) of isolated rabbit aortas. The incubation with CSE was found to inhibit EDR in a dose-dependent manner. Go-incubation of the aortic strips with superoxide dismutase (SOD), N-acetylcysteine, glutathione or dimetyl sulfoxide (DMSO), free radical scavengers, attenuated the CSE-induced inhibition of the arterial relaxation. Co-incubation of the strips with captopril (3 mM), an angiotensin converting enzyme inhibitor, also attenuated CSE-induced impairment of vasorelaxation. In parallel experiments using cultured human endothelial cells, CSE suppressed endothelial release of NOx, stable metabolites of nitric oxide (NO). SOD, DMSO and captopril attenuated the suppression of NO production by CSE in association with reduction of free radicals, superoxide anions and hydroxyl radicals, in CSE solution. Neither lactate dehydrogenase release from the cultured endothelial cells nor cell death estimated by trypan blue exclusion test was found after the incubation of the cultured endothelial cells with CSE. The results indicate that free radicals in CSE induce the impairment of EDR, which may be partly due to suppression of NO production and is not due to non specific cytotoxicity by CSE. Captopril attenuates CSE-induced endothelial dysfunction partly through scavenging free radicals. (C) 1997 Elsevier Science Ireland Ltd.