• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>Thorax >Inhaled nitric oxide and arterial oxygen tension in patients with chronic obstructive pulmonary disease and severe pulmonary hypertension
【2h】

Inhaled nitric oxide and arterial oxygen tension in patients with chronic obstructive pulmonary disease and severe pulmonary hypertension

机译：慢性阻塞性肺疾病和严重肺动脉高压患者的吸入一氧化氮和动脉血氧分压

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

BACKGROUND: Inhaled nitric oxide (NO) is a selective pulmonary vasodilator which can improve gas exchange in acute lung injury. However, it is uncertain that this effect on arterial oxygenation can be generalised to all lung diseases. METHODS: The effects of inhaled NO on gas exchange were studied in nine patients with chronic obstructive pulmonary disease (COPD), 11 patients with severe pulmonary hypertension, and 14 healthy volunteers. A randomized sequence of 40 ppm of NO or air was inhaled for 20 minutes through an orofacial mask. RESULTS: Inhaled NO reduced mean (SE) transcutaneous arterial oxygen tension (TcPO2) from 9.6 (0.3) to 8.9 (0.4) kPa in healthy volunteers and from 7.4 (0.6) to 7.0 (0.5) kPa in patients with COPD. There was no change in TcPO2 in patients with severe pulmonary hypertension. During inhalation of NO and air no change occurred in transcutaneous arterial carbon dioxide tension (TcPCO2), arterial oxygen saturation (SaO2) measured by pulse oximeter, or cardiac output determined by the transthoracic impedance method. CONCLUSIONS: Inhaled NO does not improve TcPO2 nor increase cardiac output in normal subjects and patients with COPD, suggesting that inhaled NO worsens gas exchange. This could represent inhaled NO overriding hypoxic pulmonary vasoconstriction in COPD. The finding that TcPO2 also fell when normal subjects inhaled NO suggests that a similar mechanism normally contributes to optimal gas exchange. Whilst inhaled NO can improve oxygenation, this effect should not be considered to be a general response but is dependent on the type of lung disease.


机译：背景：吸入一氧化氮（NO）是一种选择性的肺血管扩张剂，可以改善急性肺损伤中的气体交换。但是，尚不确定这种对动脉氧合的影响是否可以推广到所有肺部疾病。方法：在9例慢性阻塞性肺疾病（COPD），11例严重肺动脉高压患者和14名健康志愿者中研究了吸入NO对气体交换的影响。通过口罩吸入40 ppm NO或空气的随机序列20分钟。结果：健康志愿者的NO吸入平均经皮动脉血氧分压（SE）从9.6（0.3）降低至8.9（0.4）kPa，COPD患者从7.4（0.6）降低至7.0（0.5）kPa。严重肺动脉高压患者的TcPO2没有变化。在吸入NO和空气的过程中，经皮动脉二氧化碳张力（TcPCO2），通过脉搏血氧仪测量的动脉血氧饱和度（SaO2）或通过经胸阻抗法确定的心输出量没有变化。结论：在正常人和患有COPD的患者中，吸入NO不会改善TcPO2或增加心输出量，提示吸入NO会恶化气体交换。这可能代表了COPD中吸入的NO压倒性低氧性肺血管收缩。当正常受试者吸入NO时TcPO2也下降的发现表明，类似的机制通常有助于最佳的气体交换。虽然吸入NO可以改善氧合，但不应将其视为一般反应，而应取决于肺部疾病的类型。


著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号