CLINICAL MODELS OF THE ADULT RESPIRATORY DISTRESS SYNDROME

（摘自申请人摘要）：加州大学圣地亚哥分校/急性肺损伤SCOR的这个项目侧重于通过观察确定急性肺损伤的具体机制，使用有针对性的干预措施来预防或改善急性肺损伤。用于这些项目的人体模型包括接受肺血栓动脉内膜切除术（PT-E）的患者。高达60%的患者在pet - e后出现高通透性水肿/再灌注肺损伤。该项目的目的是通过收集来自PT-E和其他ARDS风险患者的连续血液和BALF样本，并分析这些样本中的ALI标记物[中性粒细胞和蛋白质内流，细胞因子（IL-8, tnf - α），氧化α -1蛋白酶抑制剂，谷胱甘肽水平和可溶性粘附分子（E-P-， l -选择素，ICAM-1, VCAM-1）]，继续定义这种独特的，可预测的PT-E患者肺损伤模型。三个介入试验提出了类似物，(2)使用抗氧化药物，(3)吸入一氧化氮预防再灌注肺损伤的再灌注。除了评估这三种干预措施的有效性和安全性外，还将在急性肺损伤之前、急性期和急性肺损伤消退期间收集一系列血液和支气管肺泡灌洗标本。对这些标本的分析将提供对参与急性肺损伤起始和延续的细胞成分和介质的见解。这些标本将与加州大学圣地亚哥分校其他SCOR项目的合作者共享，如果需要，也可以与其他急性肺损伤SCOR共享。（摘要结束）

(Adapted from the Applicant's Abstract): This project of the UCSD/ACUTE Lung Injury SCOR focuses on the prevention or amelioration of acute lung injury using targeted interventions based on observations which define the specific mechanisms responsible for acute lung injury. The human model used for these projects consists of patients undergoing pulmonary thromboendarterectomy (PT-E). Up to 60 percent of these patients develop a high permeability edema/reperfusion lung injury following PT-E. The aims of this project are to continue to define this unique, predictable, model of lung injury in PT-E patients by collecting sequential blood and BALF samples from PT-E and other patients at risk for ARDS and analyzing these samples for markers of ALI [neutrophil and protein influx, cytokines (IL-8, TNF-alpha), oxidized alpha1-proteinase inhibitor, glutathione levels, and soluble adhesion molecules (E-P-, L-selectins, ICAM-1, VCAM-1)]. The three interventional trials proposed analog, (2) use of an anti-oxidant drug, and (3) inhaled nitric oxide in the prevention of reperfusion of reperfusion lung injury. In addition to assessing the efficacy and safety of these three interventions, serial blood and bronchoalveolar lavage specimens will be collected prior to, during the acute phase, and during resolution of acute lung injury. Analysis of these specimens will provide insights into the cellular components and mediators that are involved in the initiation and perpetuation of acute lung injury. These specimens will be shared with collaborators working on other SCOR projects at UCSD and, if desired, with other Acute Lung Injury SCORs. (End of Abstract)