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高血压和正常血压大鼠的局部脑血流、动脉血容量及其对高碳酸血症的反应性。

Regional cerebral blood flow and arterial blood volume and their reactivity to hypercapnia in hypertensive and normotensive rats.

机构信息

Department of Radiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.

Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.

出版信息

J Cereb Blood Flow Metab. 2014 Mar;34(3):408-14. doi: 10.1038/jcbfm.2013.197. Epub 2013 Nov 20.

DOI:10.1038/jcbfm.2013.197
PMID:24252849
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3948115/
Abstract

Chronic hypertension induces cerebrovascular remodeling, changing the inner diameter and elasticity of arterial vessels. To examine cerebrovascular morphologic changes and vasodilatory impairment in early-stage hypertension, we measured baseline (normocapnic) cerebral arterial blood volume (CBV(a)) and cerebral blood flow (CBF) as well as hypercapnia-induced dynamic vascular responses in animal models. All experiments were performed with young (3 to 4 month old) spontaneously hypertensive rats (SHR) and control Wistar-Kyoto rats (WKY) under ∼1% isoflurane anesthesia at 9.4 Tesla. Baseline regional CBF values were similar in both animal groups, whereas SHR had significantly lower CBV(a) values, especially in the hippocampus area. As CBF is maintained by adjusting arterial diameters within the autoregulatory blood pressure range, CBV(a) is likely more sensitive than CBF for detecting hypertensive-mediated alterations. Unexpectedly, hypercapnia-induced CBF and blood-oxygenation-level-dependent (BOLD) response were significantly higher in SHR as compared with WKY, and the CBF reactivity was highly correlated with the BOLD reactivity in both groups. The higher reactivity in early-stage hypertensive animals indicates no significant vascular remodeling occurred. At later stages of hypertension, the reduced vascular reactivity is expected. Thus, CBF and CBV(a) mapping may provide novel insights into regional cerebrovascular impairment in hypertension and its progression as hypertension advances.

摘要

慢性高血压会引起脑血管重塑,改变动脉血管的内径和弹性。为了研究早期高血压患者的脑血管形态变化和血管舒张功能障碍,我们在动物模型中测量了基础状态(正常碳酸血症)下的脑动脉血容量(CBV(a))和脑血流(CBF),以及高碳酸血症诱导的动态血管反应。所有实验均在 9.4 Tesla 下,使用约 1%异氟烷麻醉的年轻(3 至 4 个月大)自发性高血压大鼠(SHR)和对照 Wistar-Kyoto 大鼠(WKY)进行。两组动物的基础区域 CBF 值相似,而 SHR 的 CBV(a)值明显较低,尤其是在海马区。由于 CBF 通过在自动调节血压范围内调整动脉直径来维持,因此 CBV(a)比 CBF 更能敏感地检测到高血压介导的变化。出乎意料的是,与 WKY 相比,SHR 的高碳酸血症诱导的 CBF 和血氧水平依赖性(BOLD)反应明显更高,并且两组的 CBF 反应性与 BOLD 反应性高度相关。早期高血压动物的高反应性表明没有发生明显的血管重塑。在高血压的后期阶段,预计血管反应性会降低。因此,CBF 和 CBV(a) 映射可能为高血压和高血压进展过程中的区域性脑血管损伤提供新的见解。

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