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近年有人提出一种假说,认为 ARDS 时的肺损伤是由于肺内嗜中性白细胞溶酶体蛋白酶的释放,引起弹性蛋白分解活性增强。以致损伤毛细血管内皮、基底膜和肺组织。作者为了检验这一假说而进行研究:①ARDS 组23例,平均年龄65岁,原发疾病为败血症、体外循环后、低血容量性休克等。②无ARDS 对照组:其中常态不吸烟16例;常态吸烟17例;慢性阻塞性肺疾患22例。结果 1.弹性蛋白分解活性:ARDS 组超过40U 者12例(52%);无 ARDS 对照组5例(27%)。
In recent years, people have put forward a hypothesis that the lung injury caused by ARDS is due to the release of neutrophil lysosomal proteases in the lungs, resulting in increased elastase activity. Causing damage to the capillary endothelium, basement membrane and lung tissue. In order to test this hypothesis and the study: ① ARDS group of 23 patients, mean age 65 years, the primary disease is sepsis, cardiopulmonary bypass, hypovolemic shock and so on. ② There was no ARDS control group: among them 16 were non-smoking, 17 were normal smoking and 22 were chronic obstructive pulmonary disease. Elastase activity: ARDS group more than 40U in 12 cases (52%); no ARDS control group in 5 cases (27%).