Suppr超能文献

用于研究急性二氧化氮中毒治疗的大鼠模型。

Rat model to investigate the treatment of acute nitrogen dioxide intoxication.

作者信息

Meulenbelt J, Dormans J A, Marra M, Rombout P J, Sangster B

机构信息

National Poison Control Centre, National Institute of Public Health and Environmental Protection, Bilthoven, The Netherlands.

出版信息

Hum Exp Toxicol. 1992 May;11(3):179-87. doi: 10.1177/096032719201100306.

Abstract
  1. The pulmonary toxic events induced by acute nitrogen dioxide (NO)2 exposure were studied in the rat to develop an inhalation model to investigate therapeutic measures. 2. A good correlation was observed between the lung weights and severity of the atypical pneumonitis. The pulmonary effects observed, became more pronounced with increasing NO2 concentrations (0, 25, 75, 125, 175 or 200 ppm, 1 ppm NO2 = 1.88 mg m-3 NO2) and exposure times (5, 10, 20 or 30 min). 3. An adequate NO2 concentration is 175 ppm, because it can induce a severe lung injury without mortality. This makes it possible to investigate suitable therapeutic interventions for several days. 4. Following acute inhalatory NO2 intoxication, transformation of NO2 to nitrate is presumably more notable than transformation to nitrite. 5. The transformation of NO2 to nitrate in lung tissue causes a slight increase in the serum nitrite concentration, which does not induce measurable formation of methaemoglobin. 6. Presumably, methaemoglobin does not contribute to the toxicity of NO2 intoxication.
摘要
  1. 在大鼠中研究了急性二氧化氮(NO₂)暴露引起的肺部毒性事件,以建立一种吸入模型来研究治疗措施。2. 观察到肺重量与非典型肺炎严重程度之间存在良好的相关性。随着二氧化氮浓度(0、25、75、125、175或200 ppm,1 ppm NO₂ = 1.88 mg m⁻³ NO₂)和暴露时间(5、10、20或30分钟)的增加,观察到的肺部效应变得更加明显。3. 合适的二氧化氮浓度为175 ppm,因为它可诱导严重的肺损伤而无死亡。这使得有可能在数天内研究合适的治疗干预措施。4. 急性吸入二氧化氮中毒后,二氧化氮转化为硝酸盐可能比转化为亚硝酸盐更显著。5. 肺组织中二氧化氮向硝酸盐的转化导致血清亚硝酸盐浓度略有增加,这不会诱导可测量的高铁血红蛋白形成。6. 推测高铁血红蛋白对二氧化氮中毒的毒性没有影响。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验