Weitz Z W, Birnbaum A J, Sobotka P A, Zarling E J, Skosey J L
Department of Medicine/Rheumatology, University of Illinois, Chicago.
Lancet. 1991 Apr 20;337(8747):933-5. doi: 10.1016/0140-6736(91)91569-g.
To investigate whether reperfusion after myocardial ischaemia leads to free-radical-mediated peroxidation of membrane lipids and cell damage, we measured pentane, a product of lipid peroxidation, in the breath of 10 healthy control subjects and in 20 consecutive patients with suspected acute myocardial infarction. 10 of these patients showed no myocardial damage on electrocardiography (patient control group) and 10 satisfied standard diagnostic criteria for acute myocardial infarction. The three groups were well matched for age, sex, underlying disease, and smoking habits. The time from onset of chest pain to breath collection was similar in the patient control and acute myocardial infarction groups. The breath pentane concentration was higher (p less than 0.0001) in the acute myocardial infarction group (4.96 [1.15] nmol/l) than in the patient control (1.96 [1.04] nmol/l) and healthy control groups (1.71 [0.87] nmol/l). Lipid peroxidation during acute myocardial infarction reflects action of oxygen radicals and their potential for contribution to the pathogenesis of tissue damage.
为了研究心肌缺血后的再灌注是否会导致自由基介导的膜脂质过氧化和细胞损伤,我们测量了10名健康对照者以及20名连续的疑似急性心肌梗死患者呼出气体中的戊烷(脂质过氧化产物)。这些患者中,10例心电图显示无心肌损伤(患者对照组),10例符合急性心肌梗死的标准诊断标准。三组在年龄、性别、基础疾病和吸烟习惯方面匹配良好。患者对照组和急性心肌梗死组从胸痛发作到收集呼出气体的时间相似。急性心肌梗死组的呼出气体戊烷浓度(4.96[1.15]nmol/l)高于患者对照组(1.96[1.04]nmol/l)和健康对照组(1.71[0.87]nmol/l)(p<0.0001)。急性心肌梗死期间的脂质过氧化反映了氧自由基的作用及其对组织损伤发病机制的潜在影响。