INHALED NITRIC OXIDE

吸入一氧化氮

• 批准号: 6638288
• 负责人: WARREN Myron ZAPOL
• 金额: $ 32.36万
• 依托单位: MASSACHUSETTS GENERAL HOSPITAL
• 依托单位国家: 美国
• 财政年份: 1990
• 资助国家: 美国
• 起止时间: 1990-07-01 至 2004-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6638288
• 关键词: adult respiratory distress syndrome; disease /disorder model; eicosanoid metabolism; endotoxins; enzyme activity; hyperoxia; hypoxia; laboratory mouse; nitric oxide; nonhuman therapy evaluation; oxidative stress; pulmonary hypertension; pulmonary respiration; respiratory circulation; respiratory gas level; respiratory therapy; sheep; superoxide dismutase; vascular endothelium; vasodilation

The proposal is a competitive continuation of an original grant that has led to the clinical application of inhaled nitric oxide (NO) for the treatment of pulmonary hypertension. Inhaled NO will produce selective pulmonary vasodilation IN VENTILATED alveoli in some 60% of individuals without causing a fall in arterial oxygen saturation. However, 40% of patients do noT responD to NO. The investigators will study the roles of oxygen radicals and eicosanoids in hyporesponsiveness to NO. They will determine the relationship of loss of responsiveness to NO and the loss of hypoxic pulmonary vasoconstriction (HPV) in sepsis, especially as it may relate to inducible No synthase. Lastly, they will study inhalation therapy with agents that do not affect HPV and see if they are effective in enhancing gas exchange in ovine and murine lung injury models.

该提案是对原有赠款的竞争性延续。 这导致了吸入型一氧化氮(NO)在临床上的应用 肺动脉高压的治疗。吸入NO会产生选择性 约60%无肺功能的个体在通气性肺泡内的肺血管扩张 导致动脉血氧饱和度下降。然而，40%的患者没有 回答“不”。研究人员将研究氧自由基和 二十碳酸类化合物对NO的低反应性。他们将决定这一关系 对NO的反应性丧失和缺氧性肺的丧失 脓毒症的血管收缩反应(HPV)，尤其是它可能与诱导性NO有关 合成酶。最后，他们将用不起作用的药物研究吸入疗法。 影响HPV，看看它们是否有效地促进绵羊和 小鼠肺损伤模型。