是否是心脏病发作的调解者,可以减少心脏病发作的大小,并预先调节犬类心肌?
K Przyklenk1, K Hata, R A Kloner
1Heart Institute, Hospital of the Good Samaritan, and Department of Medicine, University of Southern California, Los Angeles 90017, USA.
Circulation
|August 19, 1997
概括
注入模仿缺血预调,减少心脏病发作大小在狗. 用二甲基胺阻断的流入阻断了这种保护作用,这意味着是心脏保护的关键媒介.
科学领域:
- 心血管生理学心血管生理学
- 缺血性心脏病是一种心脏病.
背景情况:
- 缺血预先调节的细胞机制仍然不清楚.
- 被假设为心脏保护的调解者.
研究的目的:
- 为了研究在调解缺血预调的心脏病限制作用中的作用.
- 为了确定的管理是否模仿预先调节,以及通道阻断剂是否抑制其作用.
主要方法:
- 在冠状动脉封闭和再注射之前,麻醉的狗接受了冠状动脉内CaCl2或盐水.
- 测量了附带血流,风险区域 (AR) 和死区域 (AN).
- 在单独的实验中,Dimethylamiloride是一种流入抑制剂,在缺血预先调节之前被给予.
主要成果:
- 与盐溶液对照组相比,CaCl2输液显著降低了心脏病发作的大小 (AN/AR) (9+/-3%对20+/-5%).
- 甲基胺减弱了在缺血预约时观察到的心脏病发作大小减少 (12+/-1%与预约狗中的4+/-1%).
结论:
- 冠内化模仿了缺血预调的减轻心脏病发作的效果.
- 通过二甲基胺抑制流入,阻断了预条件的保护作用.
- 这些发现表明,在犬类模型中作为缺血预调节诱导的心脏保护的关键媒介.
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