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扩张型心肌病心肌细胞外基质重塑机制研究 被引量:1

Investigation of the mechanism of extracellular matrix remodelling in patients with dilated cardiomyopathy.
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摘要 目的:探讨原发性扩张型心肌病心肌细胞外基质重塑机制。方法:采用放射免疫方法测定原发性扩张型心肌病35例和24例正常对照组心肌细胞外基质血清学指标:Ⅲ型前胶原(PCⅢ)、层粘连蛋白(LN)、透明质酸(HA)以及血浆血管紧张素Ⅱ(AngⅡ)及醛固酮(ALD)含量,将AngⅡ、ALD分别与PCⅢ、LN、HA进行相关分析。结果:原发性扩张型心肌病血浆AngⅡ、ALD浓度明显增高,AngⅡ、ALD分别与PcⅢ、LN、HA密切相关。结论:原发性扩张型心肌病AngⅡ、ALD分泌明显过多,在心肌细胞外基质重塑过程中起着重要作用。 Objective: To investigate the mechanism of extracellular matrix(ECM) remodelling in patients with dilated cardiomyopathy. Methods: The concentrations of serum procollagen type Ⅲ (PC Ⅲ), laminin(LN), hyaluronic(HA) as well as plasma angiotension Ⅱ (Ang Ⅱ )and aldosterone(ALD)were measured by radioimmunoassay in 35 cases of primary dilated cardiomyopathy and 24 normal persons as control. The correlations were analysed between plasma levels of angiotension Ⅱ , aldos-terone and serum indices of ECM. Results: Compared with normal controls, the concentrations of plasma angiotension Ⅱ and aldosterone were significantly increased in primary dilated cardiomyopathy, angiotension Ⅱ positively correlated with indices of ECM,and so did afdosterone.Conclusion:Our results suggest that angiotension Ⅱ and aldosterone play important roles in ECM remodelling.
出处 《现代医药卫生》 2002年第12期1053-1054,共2页 Journal of Modern Medicine & Health
关键词 扩张型心肌病 心肌细胞外基质 重塑机制 研究 Dilated cardiomyopathy Extracellular metrix Remodelling
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参考文献4

  • 1[1]Klappacher G,Franzen P,Haab D, et al.Measuring extracel- luar matrix turnover in the serum of patients with idiopathic or ischemic dilated cardiomyopathy and impact on diagnosis and prognosis.Am J Cardiol,1995,75:913
  • 2[2]Brilla CG,Zhou GP,Matsubara,et al.Collagen metabolism in cultured adult rat cardiac fibroblasts:response to angiotension Ⅱ and aldosterione.J Mol Cell Cardiol,1994,26:809
  • 3[3]Brilla CG,Zhou GP,Rupp H,et al.Role of angiotensionⅡ and pro-staglandin E2 in regulating cardiac fibroblast collage tu- ruover.Am J cardiol,1995,76:80
  • 4[4]Sadoshima J,Izumo S.Molecular characterization of angioten- sionⅡ -induced hypertrophy of cardiac myocytes and hyper- plasia of cardiac fibroblasts:critical role of the AT1 receptor subtype.Cire Res,1993,73:413

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