CHRONIC LUNG INJURY AFTER PREMATURE BIRTH

早产后慢性肺损伤

• 批准号: 6654858
• 负责人: RICHARD David BLAND
• 金额: $ 57.92万
• 依托单位: STANFORD UNIVERSITY
• 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 2006-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6654858
• 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：（改编自研究者摘要）：支气管肺炎 发育不良是早产儿早产后长时间机械通气的并发症， 出生为了研究这种疾病的病理生理学，研究者 建立了早产羔羊BPD动物模型，3 几周的机械通气利用这个模型，生理， 生物化学、组织学和分子技术将用于确定（1） 如果不完全的肺发育对于血管和结构是必需的， 在慢性肺病中发生的肺循环异常， (2)如果吸入一氧化氮会增强NO-cGMP级联反应， 这些羔羊血管平滑肌的出生后退化，以及（3）如果 L-精氨酸的可用性降低和/或cGMP特异性 PDE导致PVR持续升高， 这些早产羔羊血管平滑肌的退化。