SCOR: ADULT RESPIRATORY FAILURE

我们计划进行一项多学科研究，对某些生化、生理和 参与急性肺损伤和修复的病理序列。 急性肺损伤的临床和实验室互补研究 威尔：阐明肺血管的最初原因和序列 严重成人呼吸窘迫综合征(ARDS)期间的损伤 血流动力学和数字减影血管造影研究以及 定量光学显微镜和超微结构分析，调查 控制肺内皮细胞细胞骨架的药物主要集中在 损伤肺细胞生物学，研究凝血系统的相互作用 并了解二十烷类化合物的代谢如何 尤其是Leokotrienes介导了肺损伤和心脏抑制。 我们计划开发新的诊断技术来测量 急性呼吸窘迫综合征的肺动脉阻抗及肺内影像 血栓形成。 我们将探讨肺气肿的基本机制和发病机制。 急性呼吸系统血栓栓塞症、血管痉挛和微血管水肿 多种病因的失败。我们希望测试一下我们新学到的知识 通过使用以下药物进行试点治疗的ARDS的机制 血栓素合成酶的溶栓、抗纤维化和抑制剂。 由于它们可能是几种肺损伤机制的核心，我们将 研究二十烷类化合物，特别是白三烯代谢 放射免疫分析和高压液相色谱检测。

We plan a multidisciplinary study of certain biochemical, physiological and pathologic sequences involved in acute lung injury and repair. Complementary clinical and laboratory investigations of acute lung injury will: elucidate the initial causes and sequences of pulmonary vascular injury during severe adult respiratory distress syndrome (ARDS) by using hemodynamic and digital subtraction angiographic studies as well as quantitative light microscopy and ultrastructural analysis, investigate agents controlling the pulmonary endothelial cell cytoskeleton focusing on injured lung cell biology, study the interaction of the coagulation system with the acutely injured lung, and learn how eicosanoid metabolities particularly the leokotrienes mediate lung injury and cardiac depression. We plan to develop new diagnostic techniques to measure the changes of pulmonary artery impedance during ARDS as well as image intrapulmonary thrombosis. We shall examine the basic mechanisms and pathogenesis of pulmonary thromboembolism, vasospasm and microvascular edema in acute respiratory failure of diverse etiology. We hope to test our newly acquired knowledge of the mechanisms of ARDS by pilot therapy with drugs that are thrombolytic, antifibrotic, and inhibitors of thromboxane synthetase. Since they may be central to several lung injury mechanisms, we will investigate eicosanoid and specifically leukotriene metabolism using radioimmunoassay and high pressure liquid chromatography.