期刊文献+

美托洛尔部分逆转心力衰竭恶病质作用的观察 被引量:1

Partial reversal of cachexia by Metoprolol therapy in patients with chronic heart failure
下载PDF
导出
摘要 目的探讨美托洛尔对心力衰竭恶病质患者体质量及血浆细胞因子水平变化的影响。方法选择心力衰竭患者分为恶病质组和非恶病质组,给予美托洛尔治疗。检测患者治疗前后体质量、血浆肿瘤坏死因子α(TNFα)、白介素1β(IL1β)和白介素6(IL6)的变化及不良事件发生率。结果治疗后两组患者血浆TNFα、IL1β和IL6较治疗前显著降低,恶病质组改变更为显著,且恶病质组体质量显著增加;治疗前后恶病质组体质量均低于非恶病质组,血浆TNFα、IL1β水平则均高于非恶病质组,IL6无显著差异。结论美托洛尔可以增加心力衰竭恶病质患者体质量,同时能降低血浆细胞因子浓度,有利于心力衰竭恶病质状态的逆转。 AIM weight and plasma To explore the effects of Metoprolol ( β-adrenergic receptor blockade) therapy on body cytokine level in chronic heart failure(CHF) patients with cachectic. METHODS The patients with CHF were divide into cachectic group and noncachectic group. Body weight, plasma tumor necrosis factor alpha( TNF-α) , interleukin-1β ( IL-1β ) , interleukin-6 ( IL-6 ) levels and incidence of adverse events were measured before and after Metoprolol therapy. RRSULTS Six months after Metoprolol therapy, subjects demonstrated significantly greater decrease in plasma TNF-α,IL-1β and IL- 6 in both groups especially in cachectic group and greater weight gain in cachectic group. Before and after therapy, subjects with cachectic demonstrated significantly lower body weight, much higher plasma TNF-α ,IL-1β and no difference in IL-6 when compared with noncachectic. CONCLUSION Metoprolol therapy is associated with body weight gain and decrease of plasma cytokine level, which is conducine to reversal of cachexia.
出处 《心脏杂志》 CAS 2006年第1期79-80,86,共3页 Chinese Heart Journal
关键词 心力衰竭 恶病质 体质量 细胞因子 美托洛尔 heart failure cachexia body weight cytokine Metoprolol
  • 相关文献

参考文献9

  • 1Anker SD,Ponikowski P,Varney S,et al.Wasting as independent risk factor for mortality in chronic heart failure[J].Lancet,1997,349:1050-1053.
  • 2Prabhu SD,Chandrasekar B,Murray DR,et al.3-Adrenergic blockade in developing heart failure:effects on myocardial inflammatory cytokines,nitric oxide,and remodeling[J].Circulation,2000,101:2103 -2109.
  • 3Deten A,Volz HC,Holzl A,et al.Effect of propranolol on cardiac cytokine expression after myocardial infarction in rats[J].Mol Cell Biochem,2003,251:127-137.
  • 4Anker SD,Sharma R.The syndrome of cardiac cachexia[J].Int J Cardiol,2002,85:51 -66.
  • 5Brink M,Anwar A,Delafontaine P.Neurohormonal factors in the development of catabolic/anabolic imbalance and cachexia[J].Int J Cardiol,2002,85:111-121.
  • 6Conraads VM,Bosmans JM,Vrints CJ.Chronic heart failure:An example of a systemic chronic inflammatory disease resulting in cachexia[J].Int J Cardiol,2002,85:33-49.
  • 7王晓明,李源,李慧芳,臧益民,贾国良.心力衰竭患者血清中TNF-α,IL-1及IL-6的变化及培哚普利对其影响[J].心脏杂志,2002,14(4):318-320. 被引量:10
  • 8Sharma AM,Pischon T,Hardt S,et al.Hypothesis:Beta-adrenergic receptor blockers and weight gain:a systematic analysis[J].Hypertension,2001,37:250-254.
  • 9Hryniewicz K,Androne AS,Hudaihed A,et al.Partial reversal of cachcxia by beta-adrenergic receptor blocker therapy in patients with chronic heart failure[J].J Card Fail,2003,9:464 -468.

二级参考文献11

  • 1Sharma R;Coats AJ;Anker SD.The role of inflammatory mediators in chronic heart failure:cytokines,nitric oxide,and endothelin-1[J],2000(02).
  • 2Francis GS.Neurohumoral activation and progression of heart failure: hypothetical and clinical considerations,1998(Suppl 1).
  • 3Mann DL.Recent insights into the role of tumor necrosis factor in the failing heart[J],2001(02).
  • 4Recchia FA;Bernstein RD;Sehgal PB.Cytokines are not a requisite part of the pathophysiology leading to cardiac decompensation[J],2000.
  • 5Dibbs Z;Kurrelmeyer K;Kalra D.Cytokines in heart failure: pathogenetic mechanisms and potential treatment,1999(05).
  • 6Wollert KC;Drexler H.The role of interleukin-6 in the failing heart[J],2001(02).
  • 7Kapadia S;Dibbs Z;Kurrelmeyer K.The role of cytokines in the failing human heart[J],1998(04).
  • 8Damas JK;Gullestad L;Aukrust P.Cytokines as new treatment targets in chronic heart failure,2001(06).
  • 9Liu L;Zhao SP.The changes of circulating tumor necrosis factor levels in patients with congestive heart failure influenced by therapy[J],1999(01).
  • 10Tsutamoto T;Wada A;Maeda K.Angiotensin II type 1 receptor antagonist decreases plasma levels of tumor necrosis factor alpha, interleukin-6 and soluble adhesion molecules in patients with chronic heart failure[J],2000(03).

共引文献9

同被引文献18

  • 1Kalogeropoulos AP, Georgiopoulou VV, Butler J. From risk factors to structural heart disease:the role of inflammation. Heart Fail Clin,2012,8:113-123.
  • 2Valgimigli M, Ceconi C, Malagutti P, et al. Tumor necrosis factor-alpha receptor 1 is a major predictor of mortality and new-onset heart failure in patients with acute myocardial infarction: the Cytokine-Activation and Long-Term Prognosis in Myocardial Infarction (C-ALPHA) study. Cir- culation ,2005,111:863-870.
  • 3Chrysohoou C, Pitsavos C, Barbetseas J, et al. Chronic systemic inflam- mation accompanies impaired ventricular diastolic function, detected by Doppler imaging,in patients with newly diagnosed systolic heart failure ( Hellenic Heart Failure Study). Heart Vessels ,2009,24:22-26.
  • 4Kawano S, Kubota T, Monden Y, et al. Blockade of NF-kappaB improves cardiac function and survival after myocardial infarction. Am J Physiol Heart Circ Physio1,2006,291 : H1337-H1344.
  • 5Frantz S,Hu K,Bayer B,et al. Absence of NF-kappaB subunit p50 im- proves heart failure after myocardial infarction. FASEB J, 2006,20: 1918-1920.
  • 6Orn S,Manhenke C, Ueland T, et al. C-reactive protein,infarct size, mi- crovascular obstruction, and left-ventricular remodelling following acute myocardial infarction. Eur Heart J,2009,30 : 1180-1186.
  • 7Pasqui AL, Di Renzo M, Maffei S, et al. Pro/Anti- inflammatory cytokine imbalance in postischemic left ventricular remodeling. Mediators ln- flamm,2010,2010:974694.
  • 8Nagai T, Anzai T, Kaneko H, et al. C-reactive protein overexpression ex- acerbates pressure overload-induced cardiac remodeling through en- hanced inflammatory response. Hypertension, 2011,57 : 208-215.
  • 9Sun M, Chen M, Dawood F, et al. Tumor necrosis factor-alpha mediates cardiac remodeling and ventricular dysfunction 'after pressure overload state. Circulation ,2007,115 : 1398-1407.
  • 10Jobe LJ, Melendez GC, Levick SP, et al. TNF-alpha inhibition attenuates adverse myocardial remodeling in a rat model of volume overload. Am J Physiol Heart Circ Physiol,2009,297 :H1462-H1468.

引证文献1

二级引证文献8

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部