Paul C. Lauterbur Research Centre for Biomedical Imaging, Shenzhen Key Laboratory for MRI, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong, China.
Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, USA.
Magn Reson Med. 2018 Mar;79(3):1602-1608. doi: 10.1002/mrm.26829. Epub 2017 Jul 21.
To determine the origins of in vivo magnetization transfer asymmetry contrast during acute ischemic stroke, particularly in the diffusion lesion, perfusion lesion, and their mismatch using a middle cerebral artery occlusion rat model of acute stroke.
Adult male Wistar rats underwent multiparametric MRI of diffusion, perfusion, T , and amide proton transfer (APT) imaging at 4.7 T following a middle cerebral artery occlusion procedure. A multipool Lorentzian model, including the nuclear Overhauser effect, magnetization transfer, direct water saturation, amine and amide chemical exchange saturation transfer effects, was applied for Z-spectrum fitting to determine the sources of in vivo magnetization transfer asymmetry following acute stroke.
We showed that changes in amine chemical exchange saturation transfer (2 ppm) and APT (3.5 ppm) effects, particularly the APT MRI effect, dominate the commonly used magnetization transfer asymmetry analysis and hence confer pH sensitivity to APT imaging of acute stroke. Also, the nuclear Overhauser effect and magnetization transfer show small changes that counteracted each other, contributing less than 0.3% to magnetization transfer asymmetry at 3.5 ppm. Moreover, we showed that diffusion lesion had worsened acidosis from perfusion/diffusion lesion mismatch (P < 0.05).
The study complements recent in vivo quantitative chemical exchange saturation transfer work to shed light on the sensitivity and specificity of endogenous APT MRI to tissue acidosis. Magn Reson Med 79:1602-1608, 2018. © 2017 International Society for Magnetic Resonance in Medicine.
利用大脑中动脉闭塞大鼠急性卒中模型,确定活体磁化转移不对称对比在急性缺血性卒中期间的起源,特别是在弥散损伤、灌注损伤及其不匹配中的起源。
成年雄性 Wistar 大鼠在大脑中动脉闭塞后,在 4.7T 进行弥散、灌注、T1 和酰胺质子转移(APT)成像的多参数 MRI。采用多池洛伦兹模型,包括核奥弗豪瑟效应、磁化转移、直接水饱和、胺和酰胺化学交换饱和转移效应,用于 Z 谱拟合,以确定急性卒中后活体磁化转移不对称的来源。
我们表明,胺化学交换饱和转移(2ppm)和 APT(3.5ppm)效应的变化,特别是 APT MRI 效应,主导着常用的磁化转移不对称分析,从而赋予急性卒中 APT 成像 pH 敏感性。此外,核奥弗豪瑟效应和磁化转移显示出相互抵消的微小变化,对 3.5ppm 的磁化转移不对称贡献小于 0.3%。此外,我们表明弥散损伤导致了灌注/弥散损伤不匹配的酸中毒恶化(P<0.05)。
本研究补充了最近的活体定量化学交换饱和转移工作,阐明了内源性 APT MRI 对组织酸中毒的敏感性和特异性。磁共振医学 79:1602-1608,2018。©2017 国际磁共振学会。