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机构地区:[1]重庆医科大学临床学院心血管内科,重庆400016
出 处:《重庆医科大学学报》2004年第4期511-512,520,共3页Journal of Chongqing Medical University
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)的浓度变化 ;观察缬沙坦对CHF患者外周血单个核细胞 (PBMC)分泌TNF -α、NO的影响 ,探讨缬沙坦治疗CHF的细胞因子机制。方法 :12例Ⅲ—Ⅳ级的CHF患者静脉血离心取PBMC ,分别加入缬沙坦和脂多糖 ,使缬沙坦终浓度为 (0、0 .0 1、0 .1、1) μmol/L ,经 2 4h孵化后 ,检测培养上清液中TNF -α、NO的浓度。结果 :CHF患者血清TNF -α、NO显著高于对照组 (P <0 .0 1)。心功能Ⅳ级组明显高于心功能Ⅲ级 (P <0 .0 1)。不同病因CHF患者之间TNF -α、NO差异无显著性。不同浓度的缬沙坦对正常人和CHF组PBMC分泌TNF -α、NO均有抑制作用 ,且随着缬沙坦浓度的升高 ,TNF -α、NO的分泌呈下降趋势。结论 :CHF的程度与TNF -α、NO浓度的相关程度提示TNF -α、NO在CHF的发生和发展中起重要作用 ,缬沙坦能够直接抑制PBMC分泌TNF -α、NO ,可能是血管紧张素Ⅱ受体拮抗剂治疗CHF的细胞因子机制之一。Objective:To examine the change of serum tumor necrosis-α (TNF-α),nitric oxide (NO) in patients with congestive heart failure(CHF) in vitro and the effect of valsartan on TNF-α production in peripheral blood mononuclear cell(PBMC),and to assess the mechanisms of valsartan in treating CHF.Methods:Venous blood sumples were obtained from both CHF patients (n=12) and healthy volunteers(n=8).Serum TNF-α and NO were measured.PBMC was obtained from both the control and the patient groups.PBMC were cultured with 0,0.01,0.1,1 μmol/L of valsartan in the presence of lipopolysaccharide.After 24 hours' incubation,TNF-α and NO were measured in the culture supernatants.Results:Serum TNF-α and NO were significantly higher than these of the control group(P<0.01),and the higher the heart failure degree,the higher the levels of the cytokines(P<0.01).Valsartan inhibited TNF-α and NO production in a concentration-dependent manner.Conclusion:TNF-α plays an important role in the development of CHF.The fact that valsartan inhibits TNF-α production in PBMC may be one of mechanisms in treating CHF by ARB.
分 类 号:R541.61[医药卫生—心血管疾病]
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