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在ARDS中急性肺损伤机理至今还不清楚,大家公认的是刺激嗜中性白细胞产生的氧自由基是引起肺损伤的中间环节。白细胞在肺毛细血管内活动和聚集、释放氧自由基攻击膜脂质的多链不饱和脂肪酸,开始过氧化反应,导致细胞膜的完整功能性丧失,使得肺泡-毛细血管的渗透性增加。肺内酶及非酶系统有防止细胞和组织的损伤作用,主要酶系统谷胱甘肽过氧化系统能除去有机和无机过氧化物毒物。巯基化合物痰易净通过巯基或谷胱甘肽的前体发挥清扫作用,此外痰易净还有解除嗜中性白细胞在肺内活化及聚集作用。按统一诊断标准选择66例ARDS病人随机分为两组:一组32例用“痰易净”治疗,另一组34例用“安慰剂”对照治疗。痰易净组在开
The mechanism of acute lung injury in ARDS is still unclear, it is acknowledged that the oxygen free radicals generated by neutrophils are the intermediate links that cause lung injury. Leukocytes in the pulmonary capillary activity and aggregation, the release of free radicals attack the membrane lipid polyunsaturated fatty acids, began peroxidation, resulting in the complete loss of cell membrane function, making alveolar capillary permeability increased. The enzymes in the lungs and non-enzymatic systems prevent cell and tissue damage. The glutathione peroxidase system, the main enzyme system, removes organic and inorganic peroxide poisons. Sulfhydryl compounds easy to purify the body through the thiol or glutathione precursors play a clear role, in addition to clear the phlegm net also lifted neutrophils in the lung activation and aggregation. Sixty-six patients with ARDS were selected according to uniform diagnostic criteria. Patients were randomly divided into two groups: one group with 32 cases treated with “Phlegm Easy” and the other 34 cases treated with “placebo”. Phlegm easy net group in the open