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Effects of iNOS-related NO on hearts exposed to liposoluble iron.

机译:iNOS相关的NO对暴露于脂溶性铁的心脏的影响。

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Inducible nitric oxide synthase (iNOS) protects heart against ischemia/reperfusion injury. However, it is unknown whether the beneficial effects of iNOS are mediated by the interaction of NO with radical oxygen species (ROS). To address this issue, we examined the effects of liposoluble iron-induced ROS generation in isolated perfused hearts from rats treated with lipopolysaccharide (LPS). LPS administration (10 mg/kg, i.p., 6 h before heart removal) induced iNOS expression and increased NO production as indicated by a 3-fold elevation of nitrite level in coronary effluents relative to control hearts. An enhanced expression of hemeoxygenase 1 protein was also observed in septic hearts compared to control. Iron-induced perfusion and contractile deficits were ameliorated by LPS with more important coronary than myocardial benefits. In iron-loaded hearts, oxidative stress as measured by the 2,3 dihydroxybenzoic acid/salicylic acid concentration ratio in cardiac tissue was 23% lower in septic than in control heart although the difference did not reach significance. In addition, the presence of the NO synthase inhibitor N-nitro-L-arginine in the perfusion medium totally blocked NO production but did not reverse the protective effects of LPS. The results indicate that LPS protects from iron-induced cardiac dysfunction by mechanisms independent on ex vivo NO production and suggest that NO acts as a trigger rather than a direct mediator of the cardioprotective effects of LPS in heart exposed to iron.
机译:诱导型一氧化氮合酶(iNOS)保护心脏免受缺血/再灌注损伤。然而,尚不清楚iNOS的有益作用是否由NO与自由基氧(ROS)的相互作用介导。为了解决这个问题,我们检查了脂多糖(LPS)处理的大鼠离体灌注心脏中脂溶性铁诱导的ROS生成的影响。相对于对照心脏,LPS给药(10 mg / kg,即在心脏摘除前6小时腹腔注射)可诱导iNOS表达并增加NO的产生,这是冠状流出物中亚硝酸盐水平提高了3倍。与对照相比,在败血性心脏中还观察到血红素加氧酶1蛋白的表达增强。 LPS改善了铁引起的灌注和收缩不足,冠心病比心肌病更重要。在铁负载的心脏中,以2,3二羟基苯甲酸/水杨酸浓度比测量的心脏组织中,氧化脓毒症的氧化应激比对照心脏低23%,尽管差异没有显着性。另外,灌注培养基中NO合酶抑制剂N-硝基-L-精氨酸的存在完全阻断了NO的产生,但没有逆转LPS的保护作用。结果表明,LPS通过独立于离体NO产生的机制来保护铁诱导的心脏功能障碍,并表明NO可以作为LPS在暴露于铁的心脏中的心脏保护作用的触发而不是直接介体。

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