CHRONIC LUNG INJURY AFTER PREMATURE BIRTH

早产后慢性肺损伤

• 批准号: 6390336
• 负责人: KURT H ALBERTINE
• 金额: $ 57.64万
• 依托单位: UNIVERSITY OF UTAH
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-09-29 至 2004-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6390336
• 关键词: apoptosis; arginine; bronchopulmonary dysplasia; disease /disorder model; enzyme activity; gene expression; guanylate cyclase; histogenesis; lung; nitric oxide; pathologic process; premature infant animal; sheep; vascular smooth muscle; vasodilation

DESCRIPTION: (Adapted from the Investigator's Abstract): Bronchopulmonary dysplasia is a complication of prolonged mechanical ventilation after premature birth. To study the pathophysiology of this disease, the investigator has developed an animal model of BPD, following premature delivery of lambs, and 3 weeks of mechanical ventilation. Utilizing this model, physiologic, biochemical, histologic, and molecular techniques will be used to determine (1) if incomplete lung development is essential for the vascular and structural abnormalities of the pulmonary circulation that occur in chronic lung disease, (2) if inhaled nitric oxide will enhance the NO-cGMP cascade and facilitate postnatal regression of vascular smooth muscle in these lambs, and (3) if decreased availability of L-arginine and/or increased activity of cGMP-specific PDE contributes to the sustained elevation of PVR and the abnormal postnatal regression of vascular smooth muscle in these premature lambs.

描述：(改编自《调查者摘要》)：支气管肺 发育不良是早产后机械通气时间延长的并发症 出生。为了研究这种疾病的病理生理学，研究人员已经 开发了早产羊羔后BPD的动物模型，以及3 几个星期的机械通风。利用这个模型，生理学的， 将使用生化、组织学和分子技术来确定(1) 如果不完全的肺发育对血管和结构的发展是必要的 慢性肺部疾病中出现的肺循环异常， (2)吸入一氧化氮可增强NO-cGMP级联反应，促进NO-cGMP的表达 这些羔羊出生后血管平滑肌的退化，以及(3)如果 L精氨酸利用率降低和/或cGMP特异性活性增加 PDE参与PVR持续升高及产后异常 这些早产羔羊的血管平滑肌退化。