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成人呼吸困难综合征(ARDS)内皮细胞通透性增强把研究工作引向细胞稳定、对抗炎症、或免疫调节机制。以往的工作提示肺微循环的作用,并选用了硫唑嘌呤(Az)来探索贫血狗在攻击肺形成组织学上的ARDS中的关系。由于Moss等的工作显示了在失血性休克后,贫血(血球压积31％)造成肺的显微镜下的病变,因而选用了贫血模型。无贫血的正常狗在出血性休克后肺部的显微病变不一致。选用肺部病变一致的模型,作者才能进行Az对肺作用的特异试验。选用杂种狗40只,平均血球压积33±2％(正常45％)。用戊巴比妥麻醉,给气管插管(带套囊的导管),
Increased endothelial cell permeability in adult dyspnoea syndrome (ARDS) leads research to cell stabilization, anti-inflammatory, or immunomodulatory mechanisms. Previous work has prompted the role of pulmonary microcirculation and selected azathioprine (Az) to explore the relationship of anemic dogs in attacking histopathology of ARDS in the lung. Since Moss et al.’s work showed microscopic lesions of the lung caused by anemia (hematocrit 31%) after hemorrhagic shock, an anemia model was chosen. Normal anemia-free dogs have heterogeneous lung lesions after hemorrhagic shock. Using a model of consistent lung disease allows the authors to perform specific tests of Az action on the lungs. 40 hybrid dogs were selected, with an average hematocrit of 33 ± 2% (normal 45%). Anesthesia with pentobarbital, intubation (catheter with cuffs)