摘要
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。
In this artical,both blood SOD activity and LPO value in 34 patients with type-Ⅱ respiratory failure and 60 healthy individuals were detected at same time.Data from our laboratory showed that PSOD and E-SOD in the patients with type-Ⅱ respiratory failure were much less than healthy individuals (P <0.001), wherase P-LPO and E-LPO value in patients with type-Ⅱ respiratory failure were much more than hedthy individuals. A Comparison of the two groups showed a significant difference (P < 0.001) as well. Authors consider that these pathophysiologlcal changes undergone hypoxemia and hemorkeological abnormalities of patients induced an increase of endogenous oxygen free radicals release, moreover, the radicals in tigarette smoke can be divided into two classes,e. g. gas phase, initiating lipid peroxidation, and tar phase, as a endogenous source of free radical that affects biological tissues through several routes.In addition,information concehang free radicals scavenging agents research aspect so far is introduced in brief.
出处
《急诊医学》
CSCD
1996年第1期19-22,共4页
关键词
呼吸衰竭
氧自由基
SOD
LPO
Respiratory failure Oxygen derived free radicals Oxygen free radicals Hypoximia Hemorheology Cigarette smoke lipid peroxidation