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)是一种可发展为 在强烈激活交感神经系统的中枢神经系统创伤后 (SNS)。该计划的长期目标是确定 SNS过度活动影响肺血的基本机制 流动和流体平衡以及这些机制如何协同工作以产生 NPE。对这些机构的了解对于设计这些机构非常重要 有效的预防和治疗措施。该项目由以下几部分组成 5项研究。研究1旨在确定是否短暂增加了 在大量SNS激活后发生的静脉回流有助于 NPE合并肺动脉高压。这将通过比较 去甲肾上腺素引起的肺动脉高压程度 麻醉犬在静脉注射的情况下给药 收益要么保持不变，要么允许增加。研究2是 旨在确定肺血管大分子筛查是如何 受伤后的能力会因高血管压力而改变 发生在NPE。这将通过评估一个 肺叶原位制备法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在肺损伤中的相对贡献 完全的血管损伤。要实现这一点，需要确定 动、静脉肺泡外血管滤过系数 分离的灌流肺叶制剂的节段被改变 气压伤。研究4旨在确定学位和时间进程 大量SNS后肺内灌注异质性发展的研究 激活。这将通过分析肺组织如何 血管和血管外运输功能(由指示器确定 稀释)脑池内注射藜芦碱产生SNS后的变化 麻醉犬体内给药情况。研究5旨在确定 如果血流不均匀是机械性的结果 肺血管压力升高或由其他SNS引起的- 诱导效应。这将通过比较肺组织的 中国动物的血管和血管外运输功能 哪些肺血管压力是机械性增加的 其中压力通过激活SNS而增加。