Lipid peroxidation and acute myocardial ischemia.
Lipid peroxidation and acute myocardial ischemia.
复制标题
脂质过氧化与急性心肌缺血。
DOI：
--
复制
发表时间：
1983
影响因子：
--
通讯作者：
Hiltrud S. Mueller
中科院分区：
文献类型：
--
作者：
Parinam S. Rao;Hiltrud S. Mueller
脂质过氧化物（LP）和自由基（FR）是急性心肌缺血过程中的代谢中间体。脂质过氧化的机制尚不清楚。我们假设：1)缺血时FR的增加是由于线粒体氧化还原状态的改变以及代谢物与O2之间的相互作用；2) FR增加了LP的形成，同时降低了保护性抗氧化剂，如谷胱甘肽过氧化物酶（GP）和抗坏血酸（ASC）。为了验证这一假设，我们首先研究了动物模型，大鼠和狗。冠状动脉闭塞（CO） 48小时后，大鼠梗死左心室组织（LV）中以丙二醛（MDA）为代表的脂质过氧化含量从0.31 nm/min/mg P增加到0.58 nm/min (P < 0.001)，增加了87%，而GP从62 nm/min/mg P减少到21 nm/min （P < 0.001）。超氧化物歧化酶含量从81µg/g降至63µg/g （p< 0.001）。多不饱和脂肪酸（PUFA）含量显著降低（花生四烯酸从19%降至16%，p< 0.001）。在狗的血液中，通过电子自旋共振光谱法研究冻干样品和儿茶酚胺（去甲肾上腺素，NE和肾上腺素，E）的顺序经心变化显示FR很早就增加。
Lipid peroxides (LP) and free radicals (FR) have recently been identified by us as metabolic intermediates during acute myocardial ischemia. The mechanism of lipid peroxidation is not clearly understood. We hypothesize: 1) FR production increases during ischemia due to alteration in the redox state of the mitochondria and due to interaction between metabolites and O2; 2) FR foster increased formation of LP with a concomitant decrease in protective antioxidants such as glutathione peroxidase (GP) and ascorbic acid (ASC). To test this hypothesis, we first studied animal models, rat and dog. In the rat, 48 hrs post coronary occlusion (CO), the lipid peroxide content in the infarcted left ventricular tissue (LV) measured as its product malondialdehyde (MDA) increased from 0.31 to 0.58 nm/ mg P (p<.001), an increase of 87% while GP decreased from 62 to 21 nm/min/mg P (p<.001). Superoxide dismutase contents decreased from 81 to 63 µg/g (p<.001). The polyunsaturated fatty acid (PUFA) contents diminished significantly (arachidonic acid from 19 to 16%, p<.001). In the dog, sequential transcardiac changes in blood showed very early increase of both FR as studied by electron spin resonance spectrometry in lyophilized samples and catecholamines (norepinephrine, NE, and epinephrine, E).