血管内皮生长因子防止了细胞亡,并保持了婴儿心脏缩的收缩功能
Ingeborg Friehs1, Rodrigo Barillas, Nikolay V Vasilyev
1Department of Cardiac Surgery, Perioperative & Pain Medicine, Children's Hospital Boston, Harvard Medical School, 300 Longwood Ave, Bader 279, Boston, Massachusetts 02115, USA.
Circulation
|July 6, 2006
概括
血管内皮生长因子 (VEGF) 治疗可以减少心脏肌肉细胞死亡. 这保护了心脏功能,并提高了压力负荷的婴儿心脏的存活率.
科学领域:
- 心血管研究研究心血管研究
- 分子生物学分子生物学
- 再生医学是一种再生医学.
背景情况:
- 心脏缩,适应工作量增加的适应性反应,可以导致心力衰竭.
- 心肌细胞亡 (编程细胞死亡) 有助于心力衰竭的进展.
- 血管内皮生长因子 (VEGF) 增强了毛细血管密度和心肌 perfusion.
研究的目的:
- 调查VEGF治疗减少心脏缩中的心肌细胞亡的假设.
- 为了确定VEGF治疗是否在压力诱导的心脏缩模型中保持心肌收缩功能.
主要方法:
- 新生子接受了大动脉带带,以诱导心脏缩.
- 过度化的动物接受了复合VEGF蛋白的腹膜内给药.
- 用TUNEL染色和PARP裂变评估心肌细胞亡;用心声扫描评估心脏功能.
主要成果:
- 与未经治疗的过度缩的心脏相比,VEGF治疗显著降低了心肌细胞亡.
- 接受VEGF治疗的动物的死亡率较低 (2/29) 与未接受治疗的动物 (14/43) 相比.
- VEGF保留了左心室质量,防止了扩张,并保持了收缩率指数.
结论:
- 心肌过度缩的毛细血管生长受损阻碍了输液和基质的输送.
- VEGF治疗减轻心肌亡,提高存活率,并保持心脏功能.
- 通过VEGF促进毛细血管生长,延迟了压力负荷的婴儿心脏中心力衰竭的发生.
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