Pathophysiologic quantities of endotoxin-induced tumor necrosis factor-alpha release in whole blood from patients with chronic heart failure
Pathophysiologic quantities of endotoxin-induced tumor necrosis factor-alpha release in whole blood from patients with chronic heart failure
复制标题
DOI：
10.1016/s0002-9149(02)02839-4
复制
发表时间：
2002-12-01
影响因子：
2.8
通讯作者：
Anker, SD
中科院分区：
文献类型：
--
作者：
Genth-Zotz, S;von Haehling, S;Anker, SD
失代偿性慢性心力衰竭（HF）患者的细菌内毒素活性升高，并作为免疫激活的有效刺激物。我们试图确定在体内观察到的活性水平（约0.6EU/ml）的内毒素是否足以刺激HF患者离体全血中肿瘤坏死因子-α（TNF-α）和TNF-α可溶性受体（sTNFR 2）的分泌。我们研究了15例HF患者（年龄65 ± 1.9岁，纽约心脏协会分级2.1 ± 0.3，左心室射血分数31 ± 5%;平均值± SEM），其中5例有心脏恶病质，7例健康对照受试者（59 ± 5岁，p = NS）。将参比内毒素以0.6、1.0和3.0 EU/ml的浓度加入静脉血中，并孵育6小时。内毒素诱导TNF-α释放呈剂量依赖性增加（p
Bacterial endotoxin activity is elevated in patients with decompensated chronic heart failure (HF) and acts as a potent stimulus for immune activation. We sought to determine whether endotoxin, at an activity level seen in vivo (around 0.6 EU/ml), is sufficient to stimulate the secretion of tumor necrosis factor-alpha (TNF-alpha) and TNF-alpha soluble receptor (sTNFR2) in ex vivo whole blood from patients with HF. We studied 15 patients with HF (aged 65 +/- 1.9 years, New York Heart Association class 2.1 +/- 0.3, left ventricular ejection fraction 31 +/- 5%; mean +/- SEM), of whom 5 had cardiac cachexia, and 7 healthy control subjects (59 +/- 5 years, p = NS). Reference endotoxin was added to venous blood at concentrations of 0.6, 1.0, and 3.0 EU/ml, and was incubated for 6 hours. Endotoxin induced a dose-dependent increase in TNF-alpha release (p