移植后的心脏缩与瘤缩因子-α的持续表达有关
S J Stetson1, A Perez-Verdia, W Mazur
1Department of Medicine, The DeBakey Heart Center, The Winters Center for Heart Failure Research, Baylor College of Medicine, Houston, Texas, USA.
Circulation
|August 8, 2001
概括
心脏全移植性缩主要是由持续的心内瘤坏死因子-α (TNF-α) 表达引起的,而不是系统性高血压. 这种细胞因子在心脏移植后有助于显著的心脏重塑.
科学领域:
- 心脏病学 心脏病学
- 免疫学 免疫学 免疫学
- 移植医学 移植医学
背景情况:
- 心脏全移植缩机制尚不清楚,但快速进展表明非血液动力学因素.
- 瘤坏死因子-α (TNF-alpha),一种在心脏全移植中发现的细胞因子,已知可诱导缩和纤维化.
- 这项研究调查了高血压,组织学变化和心肌TNF-alpha在移植后心脏缩中的作用.
研究的目的:
- 为了确定系统性高血压对心脏全移植高的贡献.
- 描述心脏移植后心脏缩的组织学决定因素.
- 评估心脏移植后心肌TNF-alpha的表达.
主要方法:
- 在心脏和肺移植接受者中,左心室质量增加与使用2D心声回声学的类似高血压率相比较.
- 分析了心肌组织样本从移植后的早期和1年的随访.
- 量化原蛋白含量 (总数,I型,III型) 和肌细胞大小.
主要成果:
- 心脏移植接受者左心室质量增加了73%,而肺移植接受者则增加了7% (P<0.0001).
- 在一年内观察到总原蛋白,原蛋白I,原蛋白III和肌细胞大小的显著增加 (P<0.0001).
- 这些组织学变化与持续的心肌TNF-alpha表达相关.
结论:
- 系统性高血压在心脏全移植缩中起的作用很小.
- 持续的心内TNF-α表达被认为是心脏全移植缩发展的关键因素.
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