【摘要】 成年大鼠暴露于>95%为O₂环境中58小时,动物死亡50%以上。外周血中红细胞内超氧化物歧化酶（Superoxide dismutasc简称SOD）活性先明显下降后上升至对照水平。外用血中白细胞计数先明显下降后也上升至对照水平。支气管肺灌洗液中细胞总数和粒细胞计数均明显升高。死前（吸入>95%O₂58小时）,支气管肺泡灌洗液中细胞总数和粒细胞数升至更高、蛋白含量和β-葡萄糖醛酸酶活性也明显升高、胸腔出现炎性积液、心重/体重明显增加。本文对高氧引起肺损伤的机理及SOD与肺损伤的关系进行了讨论。更多还原

【Abstract】 Adult Wistar rats were exposed to>95%O₂ and more than 50% experimental rats died after 58h exposure. Erythrocyte superoxide dismutase activity decreased significantly after 17h and 34h exposure and recovered after 58h exposure. Peripheral leukocyte counts decreased significantly after 10h exposure and then gradually increased to control value after 58h exposure. In bronchoalveolar lavage fluid （BALF）, the number of total cells and PMNS significantly increased after 10h, 34h, and 58h exposure. Interestingly, after 58h exposure （before death）, the total cell number, number of PMNS, protein concentration and B-glucuronidase activity in BALF suddenly increased as twice to 7 times high than after 34h exposure. Authors suggest that O₂ may be involved in the neutrophil aggregation and being sequested in lungs. The acute pulmonary inflammation may be one of the important causes of death, and alveolar macrophage may be damaged by high concentration of oxygen.更多还原