Tumour necrosis factor and inducible nitric oxide synthase in dilated cardiomyopathy
Tumour necrosis factor and inducible nitric oxide synthase in dilated cardiomyopathy
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DOI：
10.1016/s0140-6736(96)90610-8
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发表时间：
1996-04-27
期刊：
影响因子：
168.9
通讯作者：
Polak, JM
中科院分区：
文献类型：
--
作者：
Habib, FM;Springall, DR;Polak, JM
背景扩张型心肌病（DCM）的两个重要特征是心肌收缩力低下和血栓栓塞风险。一氧化氮（NO）对心肌发挥负性肌力作用，并由NO合酶产生，其诱导型（iNOS）由肿瘤坏死因子（TNF-α）刺激。方法应用组织化学和计算机图像分析技术对21例DCM或缺血性心脏病患者的心肌组织或心肌活检组织中的iNOS和TNF-α进行定量分析（IHD;结果iNOS的免疫反应性在DCM心脏的肌细胞中是强的，特别是在与内皮细胞相邻的区域，并且在DCM和IHD心脏的血管中是中等强度的，DCM患者心肌细胞iNOS免疫染色的平均光密度（0.86，范围0.21 - 1.29）大于IHD患者（0.20，范围0.095 - 0.26）（p
Background Two important features of dilated cardiomyopathy (DCM) are low myocardial contractility and risk of thromboembolism. Nitric oxide (NO) exerts a negative inotropic effect on the myocardium and is produced by NO-synthase, an inducible form of which (iNOS) is stimulated by tumour necrosis factor (TNF-alpha). Accordingly, we hypothesised that locally produced TNF-alpha might contribute to the pathogenesis and complications of DCM by inducing iNOS in the heart.Methods iNOS and TNF-alpha were quantified by histochemistry and computerised image analysis in explanted heart tissues or myocardial biopsy material from patients with DCM (n=21) or ischaemic heart disease (IHD; n=10) and from normal donor hearts (n=9).Findings Immunoreactivity for iNOS was strong in myocytes of DCM hearts, particularly in areas adjacent to the endocardium, and moderately intense in blood vessels of DCM and IHD hearts, The median optical density of the immunostaining for iNOS was greater in cardiac myocytes of patients with DCM (0.86, range 0.21 to 1.29) than in those from patients with IHD (0.20, range 0.095 to 0.26) (p