血管紧张素Ⅱ刺激心衰患者外周血单个核细胞分泌TNF-α和NO  

Angiotensin Ⅱ stimulates TNF-α and NO production in peripheral blood mononuclear cells in heart failure patients

作　　者：陈齐红[1] 覃数[1] 汪华玲[1] 肖骅[1] 

机构地区：[1]重庆医科大学附属第一医院心内科,重庆400016

出　　处：《中国病理生理杂志》2005年第6期1097-1100,共4页Chinese Journal of Pathophysiology

摘　　要：目的:检测充血性心力衰竭(CHF)患者血清肿瘤坏死因子-α(TNF-α)、一氧化氮(NO)的变化,以及血管紧张素Ⅱ(AngⅡ)、缬沙坦对培养的正常人和CHF患者单核细胞(PBMC)分泌TNF-α、NO的影响,探讨CHF时肾素血管紧张素系统与细胞因子的联系以及缬沙坦治疗CHF的细胞因子机制。方法:取16例Ⅲ-Ⅳ级的CHF患者静脉血,检测血清TNF-α、NO含量;分离PBMC,置24孔培养板中,分别加入AngⅡ,使其终浓度分别为0、0.01、0.1、1μmol/L,另外一孔加入0.1μmol/L的AngⅡ和0.1μmol/L的缬沙坦,经24h孵化后,检测培养上清中TNF-α、NO。结果:CHF患者血清TNF-α、NO水平显着高于对照组(P<0.01),心功能Ⅳ级组显著高于心功能Ⅲ级(P<0.01)。不同病因CHF患者之间TNF-α、NO含量无显著差异(P>0.05)。AngⅡ对正常人和CHF患者PBMC分泌TNF-α、NO均有促进作用,缬沙坦抑制AngⅡ诱导的PBMC分泌TNF-α、NO。结论:AngⅡ促进PBMC产生TNF-α、NO,提示肾素-血管紧张素系统与TNF-α、NO存在一定的联系,缬沙坦可能通过抑制TNF-α、NO的产生在CHF的治疗中发挥作用。AIM: To examine the change of serum tumor necrosis factor-α (TNF-α), nitric oxide (NO) in patient with congestive heart failure (CHF) and the effect of angiotensin Ⅱ (AngⅡ), valsartan on TNF-α and NO production in culture peripheral blood mononuclear cells (PBMC), to assess the relationship between the renin-angiotensin system and cytokines. METHODS: Venous blood of both healthy volunteers (n=12) and patients with CHF (n=16) were collected. Serum TNF-α and NO were examined. Peripheral blood mononuclear cells (PBMC) were obtained from both the control and the patients groups and cultured with AngⅡ at concentrations of 0, 0.01, 0.1, 1 μmol/L, respectively. AngⅡ at concentration of 0.1 μmol/L combined with 0.1 μmol/L of valsartan was also used. After 24 h incubation, the contents of TNF-α and NO in the culture supernatants were measured. RESULTS: Serum TNF-α and NO production in CHF group were significantly higher than that in control group (P<0.01). The higher the heart failure degree, the higher the levels of TNF-α and NO (P<0.01), and no significant among different etiologies of CHF (P>0.05) were observed. AngⅡ stimulated TNF-α and NO release from PBMC of patients with CHF and normal person, which was inhibited by valsartan. CONCLUSIONS: AngⅡ obviously increases TNF-α and NO production from PBMC, which indicates there is relationship between the renin-angiotensin system and TNF-α, NO. The fact that valsartan inhibits TNF-α production may be one of the mechanisms in treating CHF.

关 键 词：心力衰竭 充血性 肿瘤坏死因子 血管紧张素Ⅱ 缬沙坦 

分 类 号：R363[医药卫生—病理学]