Oxygen radical-mediated reduction in basal and agonist-evoked NO release in isolated rat heart
Oxygen radical-mediated reduction in basal and agonist-evoked NO release in isolated rat heart
复制标题
DOI：
10.1006/jmcc.2000.1334
复制
发表时间：
2001-04-01
影响因子：
5
通讯作者：
Zweier, JL
中科院分区：
文献类型：
--
作者：
Paolocci, N;Biondi, R;Zweier, JL
氧自由基 (OFR) 在缺血再灌注介导的血管功能障碍中起主要作用，这与内皮一氧化氮合酶 (eNOS) 活性的丧失相平行。作者测试了直接暴露于 OFR 是否可能通过改变一氧化氮（NO 释放）来影响血管舒张，通过氧合血红蛋白在离体大鼠心脏中监测电解 (EL) 产生的 OFR 对基础和激动剂诱发的 NO 释放的影响将电解引起的变化与用 NOS 和环加氧酶 (COX) 抑制剂 N-G-硝基-L-精氨酸甲酯 (L-NAME, 100 muM) 和吲哚美辛 (INDO, 1 mM) 灌注 30 分钟后获得的变化进行比较，通过电子顺磁反应由 O-.(2)- 和 H2O2 形成电解产生的羟基自由基 ((OH)-O-.)。共振 (EPR)，EL 后，基础 NO 释放下降 60%，冠状动脉灌注压 (CPP) 一致增加至 70%，L-NAME/INDO 灌注同样降低 NO 释放 (- 63%)，但 CPP 增加少于 EL (56 +/- 3%；P
Oxygen free radicals (OFR) play a primary role in ischemia-reperfusion-mediated Vascular dysfunction and this is paralleled by a loss of endothelial nitric oxide synthase (eNOS) activity, The authors tested whether a direct exposure to OFR may affect vascular relaxation by altering nitric oxide (NO release, Effects of electrolysis(EL)-generated OFR on basal and agonist-evoked NO release were monitored in isolated rat hearts by oxyhemoglobin assay. Electrolysis-induced changes were compared with those obtained after 30min perfusion with NOS and cyclooxygenase (COX) inhibitors N-G-nitro-L-arginine methyl ester (L-NAME, 100 muM) and indomethacin (INDO, 1 mM). Electrolysis-generated hydroxyl radical ((OH)-O-.) formed by O-.(2)- and H2O2 via the Fenton reaction as revealed by Electron Paramagnetic Resonance (EPR), After EL, basal NO release declined by 60% and coronary perfusion pressure (CPP) increased by congruent to 70%, L-NAME/INDO perfusion similarly lowered NO release (- 63%) but increased CPP less than EL (56 +/- 3%; P