在临床前心力衰竭中神经道激活. 改造和干预的可能性
G S Francis1, K M McDonald, J N Cohn
1Department of Medicine, University of Minnesota Medical School, Minneapolis.
Circulation
|May 1, 1993
概括
临床前心力衰竭涉及神经内分泌激活和左心室功能障碍. ангиотензин转化酶抑制剂可能会阻断心脏重塑,为预防心力衰竭进展提供潜在的治疗点.
科学领域:
- 心脏病学 心脏病学
- 身体生理学 身体生理学
- 病理学 病理学 病理学
背景情况:
- 充血性心力衰竭 (CHF) 通常遵循一个临床前阶段,无症状的神经内分泌激活和左心室 (LV) 功能障碍.
- 心肌损伤与交感神经系统激活,LV缩和LV体积增加有关.
- 没有受损的心脏组织显示血管激素mRNA和血管激素转化酶活性增加,这表明血管激素II在细胞生长中的作用.
研究的目的:
- 在临床前心力衰竭期间调查神经内分泌激活,LV功能障碍和心脏重塑之间的相互关系.
- 在狗模型中检查急性心肌损伤后心脏的形态和功能变化.
- 评估血管酶转化酶 (ACE) 抑制剂对心脏重塑的作用.
主要方法:
- 使用狗模型诱导急性心肌损伤.
- 在心肌损伤后监测左心室质量,体积和功能的变化.
- 评估了交感神经系统激活和神经内分泌标记物.
- 服用ACE抑制剂,以评估它们对心脏重塑的影响.
主要成果:
- 左心室质量增加是对心肌损伤的初始反应,在1周内观察到.
- 随后是渐进的交感神经系统激活,LV扩张和适度的LV功能障碍.
- 心脏重塑,包括增加 LV 质量和体积,被 ACE 抑制剂显著降低.
结论:
- 急性心肌损伤会引发一连串模仿临床前心力衰竭的事件,包括LV重塑和神经内分泌激活.
- 在心力衰竭的临床前阶段,ACE抑制显示出阻断有害重塑过程的潜力.
- 向宁-血管酶系统可能是一个可行的策略,以防止进展到明显的充血性心力衰竭.
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