EFFECTS OF PULMONARY EDEMA ON AIRWAY RESPONSIVENESS

这项提案研究了肺水肿的机制- 诱导气道反应性增加。 两种“心源性”模型 和“非心源性”肺水肿将被用于慢性 清醒的绵羊 “心源性”肺水肿将由 左心房压力（PLA）升高。 “非心源性”肺水肿 将用紫苏酮或内毒素诱导。 我们的具体 目的是解决以下问题： 1)非心源性肺水肿是否更能增加气道反应性 心源性肺水肿更严重吗 2)气道反应性的增加是否与肺动脉高压有关？ 水肿与以下情况相关： 肺水肿的严重程度？ B）肺水肿的位置？ 3)与PLA相关的气道反应性增加是否导致 发件人： A）支气管循环中血液通过时间延长？ B）静水压力增加？ 4)心源性肺水肿会长期持续吗 原因： A）气道反应性增加更大？ B）气道反应性的持续增加， 解放军恢复正常了吗？ 5)气道反应性的增加是否与肺动脉高压有关？ 水肿需要完整的支气管循环吗 6)阿托品或迷走神经阻滞是否能减轻肺水肿 增加气道反应性？ 7)肺水肿是否会增加气道对气雾剂和 静脉注射支气管收缩剂 我们很可能能够定义一个相对简单的 肺水肿的严重程度与肺动脉高压的改变之间的关系 气道反应性 对水肿与 和气道反应性应该有助于制定合理的 观察到的肺力学改变的治疗方法 充血性心力衰竭、心源性肺水肿和急性肺 损伤

This proposal examines the mechanisms responsible for pulmonary edema- induced increases in airway responsiveness. Models of both "cardiogenic" and "non-cardiogenic" pulmonary edema will be employed in chronically instrumented awake sheep. "Cardiogenic" pulmonary edema will be induced by increasing left atrial pressure (PLA). "Non-cardiogenic" pulmonary edema will be induced either with Perilla ketone or with endotoxin. Our Specific Aims are to address the following questions: 1) Does non-cardiogenic pulmonary edema increase airway responsiveness more than cardiogenic pulmonary edema? 2) Does the increase in airway responsiveness associated with pulmonary edema correlate with: A) the severity of the pulmonary edema? B) the location of the pulmonary edema? 3) Does the increased airway responsiveness associated with PLA result from: A) prolonged transit time of blood in the bronchial circulation? B) increased hydrostatic pressure? 4) Will cardiogenic pulmonary edema sustained over long periods of time cause: A) greater increases in airway responsiveness? B) more persistent increases in airway responsiveness once PLA is returned to normal? 5) Does the increase in airway responsiveness associated with pulmonary edema require an intact bronchial circulation? 6) Will atropine or vagal blockade attenuate pulmonary edema-induced increases in airway responsiveness? 7) Does pulmonary edema increase airway responsiveness to both aerosol and intravenously delivered bronchoconstrictors? It is probable that we will be able to define a relatively simple relationship between the severity of pulmonary edema and alterations in airway responsiveness. An understanding of the relationship between edema and airway responsiveness should help in the development of a rational approach to the treatment of the altered lung mechanics observed in congestive heart failure, cardiogenic pulmonary edema, and in acute lung injury.