MECHANISMS OF RESOLUTION OF NEUROGENIC PULMONARY EDEMA

神经源性肺水肿的解决机制

• 批准号: 2028136
• 负责人: MICHAEL B MARON
• 金额: $ 10.58万
• 依托单位: NORTHEAST OHIO MEDICAL UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1983
• 资助国家: 美国
• 起止时间: 1983-07-01 至 2000-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2028136
• 关键词: MECHANISMS; RESOLUTION; NEUROGENIC; PULMONARY; EDEMA

Neurogenic pulmonary edema (NPE) is a form of edema that may develop after CNS trauma that intensely activates the sympathetic nervous system (SNS). The long term objectives of this program are to determine the basic mechanisms by which such excessive SNS activity affects lung blood flow and fluid balance and how these mechanisms act in concert to product NPE. An understanding of these mechanisms is important for the design of effective preventive and treatment measures. This project is composed of 5 studies. Study 1 is designed to determine if the transient increase in venous return that occurs after massive SNS activation contributes to the pulmonary hypertension of NPE. This will be accomplished by comparing the degrees of pulmonary hypertension that develops after norepinephrine administration in the anesthetized dog under conditions where the venous return is either kept constant or allowed to increase. Study 2 is designed to determine how the pulmonary vascular macromolecular sieving capability is altered after injury by the high vascular pressures that occur in NPE. This will be accomplished by evaluating the ability of an in situ lung lobe preparation to sieve endogenous plasma proteins of varying molecular size before and after injury. Study 3 is designed to determine the relative contribution of extraalveolar vessel injury to the total vascular injury. This will be accomplished by determining how the filtration coefficients of arterial and venous extraalveolar vessel segments of an isolated perfused lung lobe preparation are altered by barotrauma. Study 4 is designed to determine the degree and time course of perfusion heterogeneity development in the lung after massive SNS activation. This will be accomplished by analyzing how the pulmonary vaScular and extravascular transport functions (determined by indicator dilution) change after SNS produced by intracisternal veratrine administration in the anesthetized dog. Study 5 is designed to determine if the perfusion heterogeneity is a consequence of the mechanical increases in pulmonary vascular pressure or results from other SNS- induced effects. This will be accomplished by comparing the pulmonary vascular and extravascular transport functions obtained from animals in which pulmonary vascular pressures are increased mechanically with those in which pressures are increased by SNS activation.

神经源性肺水肿 (NPE) 是一种可能出现的水肿形式 中枢神经系统创伤后，交感神经系统强烈激活 （社交网络）。 该计划的长期目标是确定 这种过度的 SNS 活动影响肺血的基本机制 流量和流体平衡以及这些机制如何协同作用以产生产品 NPE。 了解这些机制对于设计非常重要 采取有效的预防和治疗措施。 该项目由 5项研究。 研究 1 旨在确定是否瞬时增加 大量 SNS 激活后发生的静脉回流有助于 NPE 肺动脉高压。 这将通过比较来完成 去甲肾上腺素后发生的肺动脉高压的程度 在静脉注射的条件下对麻醉狗进行给药 回报要么保持不变，要么允许增加。 研究 2 是 旨在确定肺血管大分子筛分的方式 受伤后，由于高血管压力，能力会发生改变 发生在NPE。 这将通过评估一个人的能力来完成 原位肺叶制备以筛选内源性血浆蛋白 损伤前后分子大小不同。 研究 3 旨在 确定肺泡外血管损伤对 全血管损伤。 这将通过确定如何 动脉和静脉肺泡外血管滤过系数 分离的灌注肺叶制剂的片段被改变 气压伤。 研究 4 旨在确定学位和时间课程 大规模 SNS 后肺灌注异质性发展的影响 激活。 这将通过分析肺部如何 血管和血管外转运功能（由指标确定） 脑池内藜芦碱产生SNS后的稀释）变化 在麻醉狗中给药。 研究 5 旨在确定 如果灌注不均匀性是机械作用的结果 肺血管压力增加或其他 SNS- 的结果 诱发效应。 这将通过比较肺 从动物身上获得的血管和血管外转运功能 哪些肺血管压力会机械地增加 其中压力因 SNS 激活而增加。