N-acetylcysteine prevents pulmonary edema and acute kidney injury in rats with sepsis submitted to mechanical ventilation
N-acetylcysteine prevents pulmonary edema and acute kidney injury in rats with sepsis submitted to mechanical ventilation
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DOI：
10.1152/ajplung.00097.2011
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发表时间：
2012-04-01
影响因子：
4.9
通讯作者：
Seguro, Antonio Carlos
中科院分区：
文献类型：
--
作者：
Campos, Renata;Massola Shimizu, Maria Heloisa;Seguro, Antonio Carlos
Campos R, Shimizu MH, Volpini RA, de Bragan a AC, Andrade L, Lopes FD, Olivo C, Canale D, Seguro AC. n -乙酰半胱氨酸对机械通气脓毒症大鼠肺水肿和急性肾损伤的预防作用。[J] .中国生物医学工程杂志，2012。首次发表于2012年1月20日；doi: 10.1152 / ajplung.00097.2011。脓毒症是急性肾损伤（AKI）和急性肺损伤的常见原因。氧化应激在这种损伤中起重要作用。本研究旨在探讨强抗氧化剂n -乙酰半胱氨酸（NAC）对脓毒症大鼠肾脏和肺功能的影响。NAC（饮用水4.8 g/l）给药或不给药的大鼠在NAC给药后2天进行盲肠结扎穿刺（CLP），并持续到研究结束。CLP后24 h，观察对照组、对照组+ NAC组、CLP组和CLP + NAC组的肾功能和肺功能。所有动物均采用低潮气量机械通气。我们评估了呼吸力学、钠共转运体Na-K-2Cl （NKCC1）和上皮钠通道α亚基（α - enac）、多形核中性粒细胞、水肿指数、氧化应激（血浆硫代巴比妥酸反应性物质和肺组织8-异前列腺素）和肾小球滤过率。CLP大鼠出现AKI， CLP + NAC大鼠AKI得到改善。NAC也能改善脓毒症引起的呼吸力学改变。CLP + NAC组的水肿指数较低，肺干湿比也较低。在CLP + NAC大鼠中，α - enac表达上调，而NKCC1表达下调，但差异不显著。与CLP组相比，CLP + NAC组氧化应激显著降低，存活率显著提高。NAC的保护作用（对肾和肺损伤）可能归因于氧化应激的减少，这表明NAC可用于治疗败血症。
Campos R, Shimizu MH, Volpini RA, de Bragan a AC, Andrade L, Lopes FD, Olivo C, Canale D, Seguro AC. N-acetylcysteine prevents pulmonary edema and acute kidney injury in rats with sepsis submitted to mechanical ventilation. Am J Physiol Lung Cell Mol Physiol 302: L640-L650, 2012. First published January 20, 2012; doi: 10.1152/ajplung.00097.2011.-Sepsis is a common cause of acute kidney injury (AKI) and acute lung injury. Oxidative stress plays as important role in such injury. The aim of this study was to evaluate the effects that the potent antioxidant N-acetylcysteine (NAC) has on renal and pulmonary function in rats with sepsis. Rats, treated or not with NAC (4.8 g/l in drinking water), underwent cecal ligation and puncture (CLP) 2 days after the initiation of NAC treatment, which was maintained throughout the study. At 24 h post-CLP, renal and pulmonary function were studied in four groups: control, control + NAC, CLP, and CLP + NAC. All animals were submitted to low-tidal-volume mechanical ventilation. We evaluated respiratory mechanics, the sodium cotransporters Na-K-2Cl (NKCC1) and the alpha-subunit of the epithelial sodium channel (alpha-ENaC), polymorphonuclear neutrophils, the edema index, oxidative stress (plasma thiobarbituric acid reactive substances and lung tissue 8-isoprostane), and glomerular filtration rate. The CLP rats developed AKI, which was ameliorated in the CLP + NAC rats. Sepsis-induced alterations in respiratory mechanics were also ameliorated by NAC. Edema indexes were lower in the CLP + NAC group, as was the wet-to-dry lung weight ratio. In CLP + NAC rats, alpha-ENaC expression was upregulated, whereas that of NKCC1 was downregulated, although the difference was not significant. In the CLP + NAC group, oxidative stress was significantly lower and survival rates were significantly higher than in the CLP group. The protective effects of NAC (against kidney and lung injury) are likely attributable to the decrease in oxidative stress, suggesting that NAC can be useful in the treatment of sepsis.