INCREASED LEVELS OF SERUM NEOPTERIN AND DECREASED PRODUCTION OF NEUTROPHIL SUPEROXIDE ANIONS IN CHRONIC HEART-FAILURE WITH ELEVATED LEVELS OF TUMOR-NECROSIS-FACTOR-ALPHA
INCREASED LEVELS OF SERUM NEOPTERIN AND DECREASED PRODUCTION OF NEUTROPHIL SUPEROXIDE ANIONS IN CHRONIC HEART-FAILURE WITH ELEVATED LEVELS OF TUMOR-NECROSIS-FACTOR-ALPHA
复制标题
DOI：
10.1016/0735-1097(93)90776-w
复制
发表时间：
1993-12-01
影响因子：
24
通讯作者：
BRAUNSTEINER, H
中科院分区：
文献类型：
--
作者：
WIEDERMANN, CJ;BEIMPOLD, H;BRAUNSTEINER, H
目标.本研究的目的是探讨肿瘤坏死因子α和四氢生物蝶呤以及中性粒细胞释放超氧阴离子在严重慢性心力衰竭中的作用。以往的研究表明，在严重心力衰竭患者中，肿瘤坏死因子-α的产生增加，自由基诱导内皮细胞损伤。在基础条件下和用f-Met-Leu-Phe或佛波醇触发后，测量了16名严重心力衰竭患者和11名健康对照者的血浆和血清免疫反应性白细胞介素-1、白细胞介素、干扰素-γ、新蝶呤和肿瘤坏死因子-α水平，以及循环中性粒细胞释放的超氧阴离子。结果。与对照组相比，心力衰竭患者的肿瘤坏死因子-α和新蝶呤循环水平升高。基础和佛波酯触发的中性粒细胞释放氧自由基在心力衰竭患者中不受影响。然而，甲酰肽刺激的中性粒细胞释放的氧自由基显着减少。肿瘤坏死因子-α水平升高的心力衰竭患者中性粒细胞功能抑制可能表明对中性粒细胞衍生氧自由基有害作用的自我保护。通过诱导四氢生物蝶呤的合成（如新蝶呤增加所反映的），肿瘤坏死因子α可能影响一氧化氮的合成。
Objectives. The purpose of this study was to examine the role of tumor necrosis factor alpha and tetrahydrobiopterin and superoxide anion release from neutrophils in severe chronic heart failure.Background. Previous studies have demonstrated elevated production of tumor necrosis factor-alpha and free radical-induced endothelial cell damage in severe heart failure.Methods. Plasma and serum levels of immunoreactive interleukin-l, interleukins, interferon-gamma, neopterin and tumor necrosis factor-alpha and the release of superoxide anions from circulating neutrophils both at basal conditions and after triggering with f-Met-Leu-Phe or phorbol U-myristate If-acetate were measured in 16 patients with severe heart failure and in 11 healthy control subjects.Results. Circulating levels of tumor necrosis factor-alpha and neopterin were elevated in patients with heart failure compared; with values in control subjects. A significant correlation between the two was found. Basal and phorbolester triggered release of oxygen radicals from neutrophils was not affected in patients with heart failure. However, formylpeptide-stimulated release of oxygen radicals by neutrophils was significantly reduced.Conclusions. Suppressed neutrophil function in patients with heart failure exhibiting elevated levels of tumor necrosis-alpha factor may indicate self-protection against the deleterious effects of neutrophil derived oxygen radicals. Through induction of tetrahydrobiopterin synthesis (as reflected by increased neopterin), tumor necrosis factor alpha may affect nitric oxide synthesis.