首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Reduced microvascular volume and hemispherically deficient vasoreactivity to hypercapnia in acute ischemia: MRI study using permanent middle cerebral artery occlusion rat model
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Reduced microvascular volume and hemispherically deficient vasoreactivity to hypercapnia in acute ischemia: MRI study using permanent middle cerebral artery occlusion rat model

机译:急性缺血时微血管容量减少和对高碳酸血症的半球性血管反应不足:使用永久性大脑中动脉阻塞大鼠模型的MRI研究

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摘要

Vasoreactivity to hypercapnia has been used for assessing cerebrovascular tone and control altered by ischemic stroke. Despite the high prognostic potential, traits of hypercapnia-induced hemodynamic changes have not been fully characterized in relation with baseline vascular states and brain tissue damage. To monitor cerebrovascular responses, T2- and T2*-weighted magnetic resonance imaging (MRI) images were acquired alternatively using spin- and gradient-echo echo plannar imaging (GESE EPI) sequence with 5% CO2 gas inhalation in normal (n =5) and acute stroke rats (n=10). Dynamic relative changes in cerebrovascular volume (CBV), microvascular volume (MW), and vascular size index (VSI) were assessed from regions of interest (ROIs) delineated by the percent decrease of apparent diffusion coefficient (ADC). The baseline CBV was not affected by middle cerebral artery occlusion (MCAO) whereas the baseline MW in ischemic areas was significantly lower than that in the rest of the brain and correlated with ADC. Vasoreactivity to hypercapnic challenge was considerably attenuated in the entire ipsilesional hemisphere including normal ADC regions, in which unsolicited, spreading depression-associated increases of CBV and MW were observed. The lesion-dependent inhomogeneity in baseline MW indicates the effective perfusion reserve for accurately delineating the true ischemic damage while the cascade of neuronal depolarization is probably responsible for the hemispherically lateralized changes in overall neurovascular physiology.
机译:高碳酸血症的血管反应性已用于评估脑血管紧张度和缺血性卒中改变的控制。尽管有较高的预后潜力,高碳酸血症引起的血流动力学改变的特征尚未与基线血管状态和脑组织损伤相关地充分表征。为了监测脑血管反应,交替使用T2-和T2 *加权磁共振成像(MRI)图像,使用自旋和梯度回波回波平面成像(GESE EPI)序列,正常情况下吸入5%CO2气体(n = 5)和急性中风大鼠(n = 10)。从感兴趣区域(ROI)评估脑血管体积(CBV),微血管体积(MW)和血管大小指数(VSI)的动态相对变化,用表观扩散系数(ADC)的降低百分比来描述。基线CBV不受大脑中动脉闭塞(MCAO)的影响,而缺血区域的基线MW则显着低于大脑其他部位,并且与ADC相关。在包括正常ADC区域的整个同侧半球中,对高碳酸血症挑战的血管反应性显着减弱,在该区域中,观察到了自发性,分散性抑郁相关的CBV和MW升高。基线MW的依赖于病灶的不均匀性表明有效的灌注储备,以准确地描述真正的缺血性损伤,而神经元去极化的级联可能是整个神经血管生理学的半球侧向变化的原因。

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