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A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
Published on: July 17, 2012
冬眠触发器和心肌保护
S F Bolling1, M B Benedict, N L Tramontini
1Section of Thoracic Surgery, University of Michigan Medical Center, Ann Arbor, USA. sbolling@umich.edu
Circulation
|December 16, 1998
概括
冬眠动物的冬眠诱导触发器 (HIT) 保护子的心脏免受缺血-再输液损伤. 施用HIT改善了功能恢复,并保留了超结构形态,这表明了潜在的治疗应用.
科学领域:
- 心脏病学 心脏病学
- 生理学 生理学 生理学
- 生物化学 生物化学
背景情况:
- 低温心肌提供肌细胞保护,但后血性功能障碍仍然存在.
- 冬眠诱导触发器 (HIT),冬眠动物的一个因素,诱导冬眠,并保护免受缺血-再输液损伤.
- 了解HIT的心脏保护机制对于改善缺血后心脏恢复至关重要.
研究的目的:
- 为了研究冬眠诱导触发器 (HIT) 在缺血-再输血损伤中的心脏保护作用.
- 为了确定HIT的管理是否改善了全球性缺血后的心肌恢复.
- 探索代谢变化的潜在作用在HIT的保护作用.
主要方法:
- 隔离的子心脏在34°C的温度下接受了2小时的全球性缺血.
- 心脏接受了标准心脏,心脏中的HIT或HIT预输液.
- 在体内用HIT进行预治疗,以评估代谢改变的影响.
- 对比了后血性功能恢复 (发达的压力,冠状动脉流量,MVO2) 和超结构形态.
主要成果:
- 与车辆相比,HIT预处理显著增强了功能恢复,改善了开发的压力和冠状动脉流量.
- 超结构形态被保留在体内HIT预处理.
- HIT并没有增加肝蛋白含量,排除了简单的蛋白质新合成机制.
- 时间分析表明,一个不活跃的HIT前因子被激活了.
结论:
- 来自冬眠动物的血清 (HIT) 保护子的心脏免受缺血-再输血损伤.
- HIT的使用改善了心肌功能恢复,并保持了组织形态.
- 需要进一步的研究来确定HIT并阐明其治疗开发的保护机制.
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