摘要
心肌炎通常由病毒感染引起 ,有证据表明心肌炎最终发展成扩张性心肌病 ,是发达国家主要致死的原因。越来越多的人认为细胞因子在心肌炎和心肌病发病中起重要作用。心力衰竭病人血循环中细胞因子水平较正常人高。已证明多种细胞因子能在体内外抑制心肌收缩。细胞因子由活化的免疫细胞产生 ,它可诱生NO合酶 ,继而产生NO。已证明NO既有利又有害 ,关键在于产生NO量的多少 ,NO能抑制病毒复制 ,而保护心脏抗柯萨奇B病毒感染。无论是病毒感染对心脏的直接作用 ,还是免疫应答的利弊平衡 。
Myocarditis is thought to be commonly caused by various viruses, and accumulating evidence links viral myocarditis with the eventual development of dilated cardiomyopathy.Heart disease is the most prevalent cause of morbidity and mortality in developed countries. Cytokines are being increasingly recognized as an improtant factor in the pathogenesis of myocarditis and cardiomyopathy. Elevated levels of circulating cytokines have been reported in patients with heart failure, and various cytokines have been shown to depress myocardial contractility in vitro and in vivo. A number of reports have shown that cytokines generated by activated immune cells cause an increase in nitric oxide (NO) via induction of NO synthase. Increased generation of NO may induce myocardial damage. It has been suggested that NO can be either beneficial or harmful to the host, NO can protect the myocardium against damage from CVB3 infection by inhibiting viral replication. A better molecular understanding of the direct effect of viral infection on cardiac myocytes and the balance of beneficial and detrimental effects of the immune response will ultimately provide insight into the mechanisms by which viral infections cause cardiomyopathy in humans
出处
《生理科学进展》
CAS
CSCD
北大核心
2002年第1期30-37,共8页
Progress in Physiological Sciences