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作者同时检测了Ⅱ型呼吸衰竭病人组34例和正常对照组60例血液SOD活性和LPO含量。结果表明，病人组的P－SOD、E－SOD活性明显低于对照组，而病人组的P－LPO、E－LPO则明显高于对照组，两者相比，均存在显著差异（P＜0．001）．作者认为，低氧血症以及血液流变学和其他病理生理学上的改变，使内源性氧自由基释放增加；而抽吸烟草的烟雾中的自由基有气相（gasphase）与焦油相（tarphase）之分，经反应亦生成氧自由基，为外源性氧自由基的来源，亦能起动脂质过氧化作用，通过几个途径，影响生物组织。此外，有关当前自由基清除剂研究动态方面亦作一扼要介绍。
The authors also tested blood SOD activity and LPO content in 34 patients with type II respiratory failure and 60 normal controls. The results showed that the activity of P-SOD and E-SOD in patient group was significantly lower than that in control group, but P-LPO and E-LPO in patient group were significantly higher than those in control group (P < 0.001). The authors argue that hypoxemia, as well as hemorheology and other pathophysiological changes, increase the release of endogenous oxygen free radicals while the free radicals in the smoking tobacco smoke have a gasphase and tarphase ) Of the points, the reaction also generates oxygen free radicals, as a source of exogenous oxygen free radicals, but also start lipid peroxidation, through several channels, affecting biological tissue. In addition, there is a brief introduction on the current research status of free radical scavengers.