Acute myocardial infarction induces hypothalamic cytokine synthesis
Acute myocardial infarction induces hypothalamic cytokine synthesis
复制标题
DOI：
10.1152/ajpheart.01072.2003
复制
发表时间：
2004-06-01
影响因子：
4.8
通讯作者：
Felder, RB
中科院分区：
文献类型：
--
作者：
Francis, J;Chu, Y;Felder, RB
急性心肌梗死（MI）的炎症环境在理论上有利于脑内细胞因子合成的增强。我们检验了一个假设，即心肌梗死后脑内肿瘤坏死因子-α（TNF-α）的合成增加，TNF-α是促炎细胞因子活性的指标。通过结扎大鼠冠状动脉左前降支诱导MI，并通过超声心动图证实。使用ELISA测量TNF-α的血浆和组织水平;使用实时PCR测量TNF-α mRNA。心肌梗死后0.5、1、4、24小时或4周采集心脏、脑和血浆样本。在MI后数分钟至数小时内，脑、心脏和血浆中TNF-α的合成增加，并在测试间隔内持续。在检查的脑组织中，TNF-α选择性地在下丘脑中增加。用戊氨酰茶碱长期治疗可防止MI后4周测量的脑、心脏和血浆中TNF-α的增加。心肌梗死诱导的下丘脑细胞因子合成以及己酮可可碱对其的预防在心肌梗死后心力衰竭的发展中具有重要意义。
The inflammatory milieu of acute myocardial infarction (MI) is theoretically conducive to enhanced cytokine synthesis within the brain. We tested the hypothesis that synthesis of tumor necrosis factor-alpha (TNF-alpha), an indicator of proinflammatory cytokine activity, increases in brain after MI. MI was induced in rats by ligating the left anterior descending coronary artery and confirmed by echocardiography. Plasma and tissue levels of TNF-alpha were measured using ELISA; TNF-alpha mRNA was measured with real-time PCR. Heart, brain, and plasma samples were obtained 0.5, 1, 4, or 24 h or 4 wk after MI. TNF-alpha synthesis increased in the brain, heart, and plasma within minutes to hours after MI and was sustained over the interval tested. Among the brain tissues examined, TNF-alpha increased selectively in hypothalamus. Chronic treatment with pentoxifylline prevented the increases in TNF-alpha in brain, heart, and plasma measured 4 wk after MI. MI-induced cytokine synthesis in the hypothalamus and its prevention by pentoxifylline have important implications in the context of the development of heart failure after MI.