EFFECTS OF PULMONARY EDEMA ON AIRWAY RESPONSIVENESS

这项提案研究了导致肺水肿的机制- 诱导的呼吸道反应性增加。两种“心源性”的模型 和“非心源性”肺水肿将被长期用于 有仪表盘的清醒的绵羊。“心源性”肺水肿将由以下因素引起 增加左房内压(LA)。“非心源性”肺水肿 将被紫苏酮或内毒素诱导。我们的特定 目标是解决以下问题： 1)非心源性肺水肿是否更能增加呼吸道反应性 而不是心源性肺水肿？ 2)气道反应性的增加是否与肺相关 浮肿与以下因素有关： A)肺水肿的严重程度？ B)肺水肿的位置？ 3)与解放军相关的气道反应性增加是否会导致 出发地： A)血液在支气管循环中的转运时间延长？ B)静水压力增加？ 4)心源性肺水肿会持续很长时间吗？ 原因： A)更大程度地提高了呼吸道反应性？ B)更持久地增加一次呼吸道反应性 解放军恢复正常了吗？ 5)呼吸道反应性的增加是否与肺相关 浮肿需要完整的支气管循环吗？ 6)阿托品或迷走神经阻断能减轻肺水肿吗？ 呼吸道反应性增加？ 7)肺水肿是否增加了呼吸道对气雾剂和 静脉注射的支气管缩窄器？ 我们很可能能够定义一个相对简单的 肺水肿严重程度与肺泡灌洗液改变的关系 呼吸道反应性。对水肿病关系的认识 而呼吸道反应性应该有助于发展理性的 慢性阻塞性肺疾病肺力学改变的治疗探讨 充血性心力衰竭、心源性肺水肿和急性肺病 受伤。

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.