Mitigation of chlorine gas lung injury in rats by postexposure administration of sodium nitrite.
Mitigation of chlorine gas lung injury in rats by postexposure administration of sodium nitrite.
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通过亚硝酸钠暴露后给药减轻大鼠氯气肺损伤。
DOI：
10.1152/ajplung.00278.2010
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Matalon,Sadis
中科院分区：
文献类型：
--
作者：
Yadav,AmitK;Doran,StephenF;Samal,AndreyA;Sharma,Ruchita;Vedagiri,Kokilavani;Postlethwait,EdwardM;Squadrito,GiuseppeL;Fanucchi,MichelleV;Roberts2nd,LJackson;Patel,RakeshP;Matalon,Sadis
亚硝酸盐（NO2−）已被证明在各种缺血再灌注损伤模型中限制对心脏，肝脏和肾脏的损伤。系统性NO2−在限制肺损伤或增强修复方面的潜在保护作用尚未得到证实。我们评估了大鼠实验后腹腔注射NO2−减轻氯（Cl 2）诱导的肺损伤的有效性和机制。将大鼠暴露于Cl 2（400 ppm）30 min，然后返回室内空气中。在暴露后10 min和2、4和6 h腹腔内给予NO2−（1 mg/kg）或生理盐水。在6或24 h处死大鼠。通过定量形态学、蛋白质浓度、支气管肺泡灌洗液（BAL）中的细胞数和肺湿/干重量比评估气道和肺泡上皮的损伤。通过测量肺F2-异前列腺素评估脂质过氧化。大鼠出现严重但短暂的低氧血症。暴露后6 h，BALF中蛋白质浓度、中性粒细胞数量、气道上皮细胞数量和肺湿干重比均显著增加。定量形态学显示上呼吸道有广泛的肺损伤。气道上皮细胞末端脱氧核苷酸介导的dUTP缺口末端标记（TUNEL）染色阳性，但caspase-3不阳性。NO2-的施用导致BAL蛋白水平降低，TUNEL阳性细胞的强度显著降低，肺湿干重比正常。在NO2−和盐水注射大鼠中，暴露于Cl 2后6和24 h，F2-异前列烷水平升高。这是首次证明全身NO2−给药可减轻气道和上皮损伤。
Nitrite (NO2−) has been shown to limit injury to the heart, liver, and kidneys in various models of ischemia-reperfusion injury. Potential protective effects of systemic NO2−in limiting lung injury or enhancing repair have not been documented. We assessed the efficacy and mechanisms by which postexposure intraperitoneal injections of NO2−mitigate chlorine (Cl2)-induced lung injury in rats. Rats were exposed to Cl2(400 ppm) for 30 min and returned to room air. NO2−(1 mg/kg) or saline was administered intraperitoneally at 10 min and 2, 4, and 6 h after exposure. Rats were killed at 6 or 24 h. Injury to airway and alveolar epithelia was assessed by quantitative morphology, protein concentrations, number of cells in bronchoalveolar lavage (BAL), and wet-to-dry lung weight ratio. Lipid peroxidation was assessed by measurement of lung F2-isoprostanes. Rats developed severe, but transient, hypoxemia. A significant increase of protein concentration, neutrophil numbers, airway epithelia in the BAL, and lung wet-to-dry weight ratio was evident at 6 h after Cl2exposure. Quantitative morphology revealed extensive lung injury in the upper airways. Airway epithelial cells stained positive for terminal deoxynucleotidyl-mediated dUTP nick end labeling (TUNEL), but not caspase-3. Administration of NO2−resulted in lower BAL protein levels, significant reduction in the intensity of the TUNEL-positive cells, and normal lung wet-to-dry weight ratios. F2-isoprostane levels increased at 6 and 24 h after Cl2exposure in NO2−- and saline-injected rats. This is the first demonstration that systemic NO2−administration mitigates airway and epithelial injury.
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影响因子：
3.9
作者：
Rubbo, H;Parthasarathy, S;Freeman, BA
通讯作者：
Freeman, BA
DOI：
10.1073/pnas.88.11.4651
发表时间：
1991-06-01
影响因子：
11.1
作者：
KUBES, P;SUZUKI, M;GRANGER, DN
通讯作者：
GRANGER, DN
影响因子：
20.3
作者：
Crawford, JH;Isbell, TS;Patel, RP
通讯作者：
Patel, RP
DOI：
--
发表时间：
1969
期刊：
American Review of Respiratory Disease
影响因子：
--
作者：
H. Weill;R. George;M. Schwarz;M. Ziskind
通讯作者：
M. Ziskind
DOI：
10.1016/j.ajem.2007.12.006
发表时间：
2009-01
期刊：
The American journal of emergency medicine
影响因子：
--
作者：
Van Sickle D;Wenck MA;Belflower A;Drociuk D;Ferdinands J;Holguin F;Svendsen E;Bretous L;Jankelevich S;Gibson JJ;Garbe P;Moolenaar RL
通讯作者：
Moolenaar RL