Arteaga Daniel F, Strother Megan K, Faraco Carlos C, Jordan Lori C, Ladner Travis R, Dethrage Lindsey M, Singer Robert J, Mocco J, Clemmons Paul F, Ayad Michael J, Donahue Manus J
Department of Radiology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Department of Neurology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
J Cereb Blood Flow Metab. 2014 Sep;34(9):1453-62. doi: 10.1038/jcbfm.2014.106. Epub 2014 Jun 11.
'Vascular steal' has been proposed as a compensatory mechanism in hemodynamically compromised ischemic parenchyma. Here, independent measures of cerebral blood flow (CBF) and blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) responses to a vascular stimulus in patients with ischemic cerebrovascular disease are recorded. Symptomatic intracranial stenosis patients (n=40) underwent a multimodal 3.0T MRI protocol including structural (T1-weighted and T2-weighted fluid-attenuated inversion recovery) and hemodynamic (BOLD and CBF-weighted arterial spin labeling) functional MRI during room air and hypercarbic gas administration. CBF changes in regions demonstrating negative BOLD reactivity were recorded, as well as clinical correlates including symptomatic hemisphere by infarct and lateralizing symptoms. Fifteen out of forty participants exhibited negative BOLD reactivity. Of these, a positive relationship was found between BOLD and CBF reactivity in unaffected (stenosis degree<50%) cortex. In negative BOLD cerebrovascular reactivity regions, three patients exhibited significant (P<0.01) reductions in CBF consistent with vascular steal; six exhibited increases in CBF; and the remaining exhibited no statistical change in CBF. Secondary findings were that negative BOLD reactivity correlated with symptomatic hemisphere by lateralizing clinical symptoms and prior infarcts(s). These data support the conclusion that negative hypercarbia-induced BOLD responses, frequently assigned to vascular steal, are heterogeneous in origin with possible contributions from autoregulation and/or metabolism.
“血管盗血”被认为是血流动力学受损的缺血实质中的一种代偿机制。在此,记录了缺血性脑血管病患者对血管刺激的脑血流量(CBF)和血氧水平依赖(BOLD)磁共振成像(MRI)反应的独立测量值。有症状的颅内狭窄患者(n = 40)在室内空气和高碳酸血症气体吸入期间接受了多模态3.0T MRI检查,包括结构成像(T1加权和T2加权液体衰减反转恢复序列)以及血流动力学成像(BOLD和CBF加权动脉自旋标记)功能MRI。记录了显示负BOLD反应性区域的CBF变化,以及包括梗死所致有症状半球和定位症状在内的临床相关因素。40名参与者中有15名表现出负BOLD反应性。其中,在未受影响(狭窄程度<50%)的皮层中,BOLD和CBF反应性之间存在正相关关系。在负BOLD脑血管反应性区域,3例患者的CBF出现显著(P<0.01)降低,符合血管盗血;6例患者的CBF增加;其余患者的CBF无统计学变化。次要发现是,负BOLD反应性与通过定位临床症状和既往梗死确定的有症状半球相关。这些数据支持以下结论:高碳酸血症诱导的负BOLD反应(常归因于血管盗血)起源异质性,可能与自动调节和/或代谢有关。