机械卸载与神经幽默刺激对心肌结构和内分泌功能的影响 In vivo
O Lisy1, M M Redfield, S Jovanovic
1Division of Cardiovascular Diseases, Departments of Internal Medicine and Physiology, Mayo Clinic and Foundation, Rochester, MN, USA. lisy.ondrej@mayo.edu
Circulation
|July 19, 2000
概括
慢性心脏卸载导致心肌缩和心房 natriuretic (ANP) 合成减少,尽管增加了神经幽默刺激. 这项研究澄清了机械负荷.
科学领域:
- 心血管生理学心血管生理学
- 心脏内分泌学心脏内分泌学
背景情况:
- 机械负荷和幽默因子,如内甲蛋白 (ET) 和血管素II (Ang II),显著影响心脏结构和功能.
- 耳前 natriuretic (ANP) 基因表达,产生和释放是由这些刺激调节的.
- 了解机械卸载和神经道激活在ANP之间的相互作用至关重要.
研究的目的:
- 研究慢性机械卸载对心肌和循环ANP水平的影响.
- 为了比较机械卸载与神经道刺激 in vivo 的效果.
- 阐明胸下静脉缩 (TIVCC) 在调节心脏ANP中的作用.
主要方法:
- 胸下静脉缩 (TIVCC) 在狗身上进行了10天,以诱导慢性心肌卸载.
- 评估了血液动力学参数,血ET和Ang II水平以及心肌标志物.
- 分析了左心室 (LV) 质量,肌细胞尺寸,心房ANP储量,血ANP和ANP基因表达.
主要成果:
- TIVCC导致心脏输出量降低,右心房压和LV终端-透气直径.
- 观察到显著的血和心肌ET和AngII的激活.
- 尽管神经道激活,但LV质量和肌细胞直径下降 (缩),心房ANP储量增加,但血ANP和基因表达没有显著变化.
结论:
- 心脏的慢性机械卸载导致心肌缩.
- 尽管有ET和AngII的显著神经幽默刺激,但ANP的合成和释放没有被激活.
- 机械卸载取代了关于ANP调节的强有力的促进生长的神经幽默信号.
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