在体内过渡性缺血期间心肌甲醇胺释放的时间过程和机制
T W Lameris1, S de Zeeuw, G Alberts
1Department of Internal Medicine I, Cardiovascular Research Institute COEUR, Erasmus University Rotterdam, Rotterdam, The Netherlands. TWL@mediaport.org
Circulation
|June 7, 2000
概括
心肌缺血显著提高心肌间歇性液 (MIF) 中的甲醇胺,部分由逆向神经回收驱动. 这表明功能性交感神经终端即使在心脏病发作后仍然存在.
科学领域:
- 心脏病学 心脏病学
- 神经科学是一个神经科学.
- 生理学 生理学 生理学
背景情况:
- 在缺血性心肌中观察到高上腺素 (NE).
- 在缺血和再注射期间,研究心肌间歇液 (MIF) 中的甲基荷胺释放机制至关重要.
研究的目的:
- 确定心肌缺血和再注血期间MIF中甲醇胺释放的数量和机制.
- 阐明神经元再吸收在心脏缺血期间 катехолами因释放中的作用.
主要方法:
- 在麻醉后的猪中使用微透析来测量间歇性类甲醇胺度.
- 由左前下垂冠状动脉 (LAD) 堵塞60分钟引起的区域性心肌缺血,随后进行150分钟的再输血.
- 在闭塞后的最后30分钟内服用提拉胺,以评估神经元释放能力.
主要成果:
- 在MIF中,在闭塞期间,在缺血区域中,诺亚上腺素,多巴胺和上腺素度显著增加.
- 局部吸收-1 阻断可以将甲基荷兰胺释放量降低50%以上.
- 在再注血过程中,MIF类甲醇胺水平恢复到基线,而胺诱导的NE释放在心脏病发作的组织中保持不变.
结论:
- 心肌缺血导致MIF类甲醇胺的显著增加,部分原因是神经元反向重新吸收.
- 增加MIF上腺素表明心脏神经元源.
- 维护了对氨酸的甲基荷兰胺反应,表明在后缺血性心肌中具有功能性的交感神经末端.
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