近年来,越来越多的研究表明,具有高度活性的氧自由基(OFR—S)是导致许多疾病病理过程中组织细胞损伤的重要因素。许多学者发现,急性呼吸窘迫综合征(ARDS)的发生与中性粒细胞在肺内的聚集有关,而聚集的白细胞被激活后发生“呼吸爆发”时,可产生并释放大量氧自由基,从而导致许多病理过程。用药物增强机体对自由基的清除功能或是保护细胞免受自由基损伤,乃是当前治疗中的重要问题之一。本实验采用内毒素(LPS)和肿瘤坏死因子(TNF—α)协同作用,制成家兔ARDS模型,测定动物体内氧自由基清除剂超氧化物歧化酶(SOD)及脂质过氧化产物丙二醛 In recent years, more and more studies have shown that the highly active oxygen free radical (OFR-S) is an important factor leading to the damage of tissue cells in the pathological process of many diseases. Many scholars have discovered that the occurrence of acute respiratory distress syndrome (ARDS) is related to the accumulation of neutrophils in the lungs, and that when accumulated leukocytes are activated and undergo a “respiratory burst”, they can produce and release a large number of oxygen free radicals. Causes many pathological processes. The use of drugs to enhance the body’s ability to scavenge free radicals or to protect cells from free radical damage is one of the important issues in current treatments. In this study, a rabbit ARDS model was established using the synergistic action of endotoxin (LPS) and tumor necrosis factor (TNF-α) to determine the superoxide dismutase (SOD) and lipid peroxidation product C in the animal’s body. Dialdehyde