在犬冠状动脉微循环中调节剪切应力
D W Stepp1, Y Nishikawa, W M Chilian
1Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA. dstepp@post.its.mcw.edu
Circulation
|October 6, 1999
概括
冠状动脉的剪切应力由内皮中释放的氧化 (NO) 调节,特别是在小动脉中,这表明血流控制的关键机制.
科学领域:
- 心血管生理学心血管生理学
- 血管生物学 血管生物学
- 血液动力学 血液动力学
背景情况:
- 压力和流量等物理力量会影响冠状动脉血管功能.
- 剪切应激增加导致冠状动脉小动脉的血管扩张 in vitro.
- 剪切应力调节被假设为血流控制的负反机制.
研究的目的:
- 在体内研究冠状动脉循环中的剪切应力调节.
- 在基底和高流量条件下量化微血管剪切应力.
- 确定氧化 (NO) 在剪切应力调节中的作用.
主要方法:
- 使用光微血管学测量微血管直径和速度 in vivo.
- 从直径和速度测量计算的剪切应力.
- 服用腺来诱导最大的冠状动脉血流,并抑制NO合成酶.
主要成果:
- 已确定的基底剪切应力值:小动脉10dyn/cm2,小动脉19dyn/cm2.
- 在高流量时观察到小动脉的剪切应力调节,但在动脉小动脉的调节最小.
- 在血管扩张过程中,NO合成酶阻塞取消了小动脉的剪切应力调节.
结论:
- 提供了第一批对冠状动脉循环中微血管剪切应力的定量估计.
- 证明了小冠状动脉的剪切应力是由内皮中NO的释放调节的.
- 突出了内皮NO在增加血液流动期间维持剪切应激恒温的作用.
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