慢性高血压改变了附带血流,皮质大脑血流和大脑组织氧化之间的关系
Ryan D Hunt1, Marilyn J Cipolla1,2,3,4
1Department of Neurological Sciences, University of Vermont, Larner College of Medicine, Burlington, VT, USA.
概括
在急性缺血性中风中,高血压会减少大脑的血液流动和氧化. 在高血压和正常血压的老鼠中,暂时增加血压改善了这些指标.
科学领域:
- 神经科学是一个神经科学.
- 心血管科学 心血管科学
- 脑卒中研究 脑卒中研究
背景情况:
- 高血压是中风的主要危险因素.
- 了解高血压对中风期间大脑血流动力学的影响至关重要.
- 皮亚尔附带流在弥补缺血事件期间血液流量减少方面发挥着作用.
研究的目的:
- 为了研究在急性缺血性中风期间,皮层脑侧边 (leptomeningeal anastomoses,LMA) 流动,皮层脑血流 (cCBF) 和脑组织氧化 (btO2) 之间的关系.
- 为了检查这种关系是如何改变在慢性高血压的背景下.
- 评估诱导高血压对这些参数的影响.
主要方法:
- 在Wistar大鼠和自发高血压大鼠 (SHR) 中进行过渡性中脑动脉封闭 (tMCAO).
- 激光多普勒探测器测量了LMA流量,一个组合激光多普勒-氧探测器测量了btO2和cCBF在心脏梗塞前皮层.
- 乙烯被输注以诱导短暂的高血压和评估大脑血流 (CBF) 自主调节.
主要成果:
- 在tMCAO期间,SHR与Wistar老鼠相比显示出较低的btO2和cCBF,尽管LMA流量相似.
- 在Wistar大鼠中,LMA流,cCBF和btO2之间的相互依赖是完整的,但在SHR中被破坏了.
- 诱导高血压在SHR中部分恢复了被破坏的关系,并在Wistar和SHR大鼠中显示出好处.
结论:
- 慢性高血压在急性缺血性中风期间降低了cCBF和btO2.
- 涉及健康附带流的补偿机制在高血压中受损.
- 诱导性高血压在中风期间对大脑输液产生有益影响,无论基线高血压状态如何.
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