摘要
目的 探讨长期吸入一氧化氮 (NO)对慢性缺氧性肺动脉高压的影响及其毒副反应。方法 从 5 4只 Wistar大鼠 (雌雄各半 )中随机取 6只作为正常对照组 ,其余 48只常压缺氧两周复制成慢性缺氧性肺动脉高压模型后分为 :缺氧组 :每日继续缺氧 6小时 ;吸入 NO组 :继续缺氧同时每日吸入 40 ppm (4 0 / 10 6) NO1小时 ,于第 8、 15、 2 2、 2 9天分别观察肺动脉压力、右心室肥厚指标、血高铁血红蛋白含量以及肺组织病理学改变。结果 (1)缺氧组大鼠肺动脉平均压明显升高 ,右心室肥厚显著 (P均 <0 .0 1) ,而吸入 NO组肺动脉压降低 ,右心室肥厚减轻 ;(2 )吸入 NO不同时间组血高铁血红蛋白含量与缺氧组同时间及正常对照组比较无明显升高 ,且吸入 NO各时段组间比较亦无明显差异 (P >0 .0 5 ) ;(3)光镜下 ,缺氧组腺泡内肌型肺动脉增多、无肌肺动脉明显减少 ,与正常对照组及吸入 NO组比较 ,有显著差异 (P <0 .0 1) ;吸入 NO组明显改善三型血管比例失调 ,阻抑慢性缺氧所造成的腺泡内肺动脉肌化和肌型小动脉中膜增厚 ,未见明显肺泡水肿、渗出、细胞浸润等 NO损伤性改变。结论 长期吸入 40 ppm NO可以减轻大鼠慢性缺氧性肺动脉高压、右心室肥厚以及肺小血管肌化程度 。
Objective To study the effect and toxicity of prolonged inhalation of nitric oxide on chronic hypoxic pulmonary hypertensive rats Methods Wistar rats were randomly divided into three groups:(1)room air control(C);(2)hypoxia(H);(3)hypoxia with the inhalation of 40ppm NO for one hour per day (N) mPAP、RV/LV+S、MeHb and the histopathology of the lung were examined respectively on the 8th,15th,22th and 29ht day Results 1 hypoxia caused marked elevation in mPAP and RV/LV+S(P<0 01) Prolonged inhalation of nitric oxide significantly reduced mPAP and RV/LV+S compared with those in hypoxia 2 Methemoglobin levels after 7 to 28 days of inhalating 40ppm NO didn't change from control and hypoxia values(P>0 05) 3 hypoxia raised the percentage of intraacinar muscular artery (MA) and lowered that of non muscular artery(NMA)compared with the control and inhalation of NO groups(P<0 01) Prolonged inhalation of NO could inhibit the medial hypertrophy of muscular arteries and muscularization of non muscular arteries Apparent lung injuries because of prolonged inhalation of NO hadn't been found in light microscopy Conclusions prolonged inhalation of NO could lower hypoxic pulmonary hypertension and inhibit the remodelling of the IAPA and cause no apparent toxicity in chronic hypoxic pulmonary hypertensive rats
出处
《医学文选》
2001年第5期588-591,共4页
Anthology of Medicine
关键词
缺氧症
一氧化氮
肺性高血压
毒力
Anoxia
Nitric oxide
Hypertension,pulmonary
Toxicity
