Department of Experimental Biology, University of Jaen, Paraje Las Lagunillas s/n, 23071, Jaen, Spain.
J Biosci. 2011 Mar;36(1):69-78. doi: 10.1007/s12038-011-9006-4.
Nitric oxide (NO) has been reported to act both as a destructive and a protective agent in the pathogenesis of the injuries that occur during hypoxia/reoxygenation (H/R). It has been suggested that this dual role of NO depends directly on the isoform of NO synthase (NOS) involved. In this work, we investigate the role that NO derived from endothelial NOS (eNOS) plays in cardiac H/R-induced injury. Wistar rats were submitted to H/R (hypoxia for 30 min; reoxygenation of 0 h, 12 h and 5 days), with or without prior treatment using the selective eNOS inhibitor L-NIO (20 mg/kg). Lipid peroxidation, apoptosis and protein nitration, as well as NO production (NOx), were analysed. The results showed that L-NIO administration lowered NOx levels in all the experimental groups. However, no change was found in the lipid peroxidation level, the percentage of apoptotic cells or nitrated protein expression, implying that eNOS-derived NO may not be involved in the injuries occurring during H/R in the heart. We conclude that LNIO would not be useful in alleviating the adverse effects of cardiac H/R.
一氧化氮（NO）在缺氧/复氧（H/R）过程中发生的损伤的发病机制中，既被报道为一种破坏剂，也被报道为一种保护剂。有人认为，NO 的这种双重作用直接取决于所涉及的一氧化氮合酶（NOS）同工型。在这项工作中，我们研究了内皮型一氧化氮合酶（eNOS）衍生的 NO 在心脏 H/R 诱导损伤中的作用。Wistar 大鼠接受 H/R（缺氧 30 分钟；复氧 0 小时、12 小时和 5 天），同时或不事先使用选择性 eNOS 抑制剂 L-NIO（20mg/kg）进行治疗。分析了脂质过氧化、细胞凋亡和蛋白硝化以及 NO 产生（NOx）。结果表明，L-NIO 给药降低了所有实验组的 NOx 水平。然而，脂质过氧化水平、凋亡细胞百分比或硝化蛋白表达均未发生变化，这意味着 eNOS 衍生的 NO 可能不参与心脏 H/R 过程中的损伤。我们得出结论，L-NIO 对减轻心脏 H/R 的不良影响没有作用。
