卡尔西纽林被激活在老鼠心脏中,其生理左心室缩是由自愿的运动训练引发的
1Department of Cardiovascular Medicine, University of Tokyo, Japan.
Circulation
|May 10, 2000
概括
氨酸激活是运动诱导的心脏缩的关键,但不是先进的压力过载缩. 环素A阻碍了有益的适应性缩,建议谨慎使用它来预防左心室缩 (LVH).
科学领域:
- 心血管生理学心血管生理学
- 分子生物学分子生物学
- 运动科学 运动科学
背景情况:
- 卡尔西纽林在心脏缩信号中的作用受到争论,在各种实验模型中存在相互矛盾的证据.
- 了解氨酸在不同类型的左心室缩 (LVH) 中的参与对于治疗策略至关重要.
研究的目的:
- 为了比较来自自愿运动的生理性LVH与来自大动脉收缩的病理性LVH.
- 调查氨酸在运动诱导的LVH的信号通路中的参与.
主要方法:
- 威斯塔尔老鼠接受了自愿运动 (EX),久坐的饮食,上升大动脉收缩 (AC1,AC4) 或假冒手术.
- 测量了左心室 (LV) 尺寸,中风体积和心肌氨酸活性.
- 环素A对LVH发展的影响在EX和AC4组中进行了评估.
主要成果:
- 自愿性运动 (EX) 增加了 LV 透静维度和中风体积,伴随着显著增加心肌氨酸活性.
- 上升性大动脉收缩 (AC1) 也显示出氨酸活性增加,而AC4 (减补) 则没有.
- 环素A完全阻断了运动诱导的LVH,但在AC4大鼠中仅部分降低了超.
结论:
- 氨酸在生理性,运动诱导的LVH和早期病理性LVH (AC1) 中被激活,但在不补偿性缩 (AC4) 中没有被激活.
- 环素A对适应性缩的抑制表明,当用于LVH预防时,它可能会造成潜在的危害,因为它针对有益的途径.
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