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Chronic ethanol ingestion increases nitric oxide production in the lung.

机译：长期摄入乙醇会增加肺中一氧化氮的产生。

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Chronic ethanol (EtOH) ingestion increases the incidence of acute respiratory distress syndrome. The mechanisms underlying EtOH-induced susceptibility to lung injury continue to be defined. This study examines the hypothesis that EtOH increases endothelial nitric oxide synthase (eNOS) expression and activity in the lungs of a rat model of chronic EtOH ingestion. Male Sprague-Dawley rats were fed liquid diets containing EtOH (36% of calories) or maltose-dextrin as an isocaloric substitution for EtOH (control) for 6 weeks. Selected animals were also treated with the angiotensin-converting enzyme (ACE) inhibitor lisinopril (3 mg/l in diet) for 6 weeks. At study completion, animals were sacrificed, and lung tissue was collected for assays of nitric oxide (NO) metabolism or pulmonary microvascular endothelial cells (MVEC) were isolated for analysis of NO release. Compared to the control diet, chronic EtOH ingestion increased lung H2O2 production, eNOS expression and activity, lung cyclic guanosine monophosphate (cGMP) content, and levels of protein nitration and oxidation. MVEC from animals with chronic EtOH ingestion released greater amounts of NO. EtOH-induced increases in lung H2O2 production, eNOS expression and activity, cGMP content, protein nitration and oxidation, and MVEC NO production were all attenuated by treatment with lisinopril. Chronic EtOH ingestion stimulates ACE-dependent increases in NO production in the lung. These novel findings indicate that chronic EtOH ingestion increases reactive species production in the lung parenchyma and provide new insights into mechanisms by which EtOH causes phenotypic alterations in the lung and alters the lung's response to inflammatory stimuli.
机译：长期摄入乙醇（EtOH）会增加急性呼吸窘迫综合征的发生率。 EtOH诱导的肺部损伤敏感性的机制仍在确定中。这项研究检验了以下假设：EtOH会增加慢性EtOH摄入大鼠模型的肺中内皮型一氧化氮合酶（eNOS）的表达和活性。给雄性Sprague-Dawley大鼠喂食含EtOH（占卡路里的36％）或麦芽糖糊精等热量替代EtOH（对照）的流质饮食6周。选定的动物也用血管紧张素转换酶（ACE）抑制剂赖诺普利（饮食中3 mg / l）治疗6周。在研究完成时，处死动物，并收集肺组织用于一氧化氮（NO）代谢测定，或分离肺微血管内皮细胞（MVEC）用于分析NO释放。与对照饮食相比，长期摄入EtOH会增加肺中H2O2的产生，eNOS的表达和活性，肺环一磷酸鸟苷（cGMP）的含量以及蛋白质硝化和氧化的水平。长期摄入EtOH的动物的MVEC释放出更多的NO。 EtOH诱导的肺过氧化氢生成，eNOS表达和活性，cGMP含量，蛋白质硝化和氧化以及MVEC NO生成的增加均通过赖诺普利治疗而减弱。长期摄入EtOH会刺激ACE依赖的肺NO生成增加。这些新发现表明，长期摄入EtOH会增加肺实质中反应性物质的产生，并为EtOH引起肺表型改变并改变肺对炎症刺激反应的机制提供新见解。

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