High Temporal Resolution Diffusion MRI of Global Cerebral Ischemia and Reperfusion
High Temporal Resolution Diffusion MRI of Global Cerebral Ischemia and Reperfusion
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DOI：
10.1097/00004647-199609000-00013
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发表时间：
1996-09
影响因子：
6.3
通讯作者：
C. Pierpaoli;J. Alger;A. Righini;J. Mattiello;Russell Dickerson;Daryl Des Pres;A. Barnett;G. Chiro
中科院分区：
文献类型：
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作者：
C. Pierpaoli;J. Alger;A. Righini;J. Mattiello;Russell Dickerson;Daryl Des Pres;A. Barnett;G. Chiro
虽然脑缺血已被广泛研究，使用扩散加权磁共振成像，迄今为止进行的大多数研究没有足够的时间分辨率，以遵循超急性缺血的水表观扩散系数（ADC）的时间变化。使用扩散回波平面成像，我们获得了ADC图（从测量8 b值计算）的时间分辨率为43秒的猫模型的全脑缺血和再灌注。不同的协议进行：10分钟的低灌注，10分钟和22分钟的缺血再灌注，心脏骤停。从内囊的白色物质和丘脑获得ADC值。由于皮质脑沟中的CSF非常接近，因此认为皮质灰质测量结果不可靠。闭塞后，丘脑中的ADC在1.5-2.5 min内下降至其正常基线值的<2 SD。该衰减呈指数衰减，时间常数（τ ± SD）为6.0 ± 2.6 min;缺血后10 min未观察到ADC进一步下降。再灌注后，在显示ADC恢复的动物中，ADC立即开始增加，在15分钟内恢复到缺血前的值。在低灌注期间未观察到显著的ADC变化。心搏停止后，丘脑ADC值的衰减（τ = 2.6 ± 0.6 min）比白色物质（τ = 6.6 ± 1.8 min）快。我们观察到心脏停搏后40分钟的ADC与缺血后10分钟的ADC相似。考虑到所有经历10分钟缺血发作的动物均显示ADC随再灌注而恢复，怀疑是否有可能定义ADC的阈值，低于该阈值脑组织将不可逆地受损。最后，尽管由缺血诱导的ADC衰减的时间常数存在变异性，但所有动物在10 min时的ADC值非常相似。这表明，当血流减少到足以引起ADC降低时，灌注差异会影响降低的速度，但不会影响最终达到的渐近值。
Although brain ischemia has been extensively studied using diffusion-weighted magnetic resonance imaging, most studies performed so far have not had adequate time resolution to follow the temporal changes in the water apparent diffusion coefficient (ADC) in hyperacute ischemia. Using diffusion echo planar imaging, we obtained ADC maps (calculated from measurements made with 8 b-values) with a time resolution of 43 s in a feline model of global brain ischemia and reperfusion. Different protocols were performed: 10-min hypoperfusion, 10- and 22-min ischemia followed by reperfusion, and cardiac arrest. ADC values were obtained from white matter of the internal capsule and from the thalamus. Cortical gray matter measurements were not deemed reliable due to the close proximity of CSF in the cortical sulci. Following occlusion, the ADC declined in the thalamus to <2 SD of its normal baseline value within 1.5–2.5 min. This decay was exponential with a time constant (τ ± SD) of 6.0 ± 2.6 min; no further decrease in the ADC was observed 10 min following ischemia. Following reperfusion, in animals that showed ADC recovery, the ADC began increasing immediately, returning to its preischemic value in ∼15 min. No significant ADC changes were observed during hypoperfusion. Following cardiac arrest, the decay of ADC was more rapid in the thalamus (τ = 2.6 ± 0.6 min) than in white matter (τ = 6.6 ± 1.8 min). We observed that the ADC at 40 min after cardiac arrest was similar to the ADC at 10 min after ischemia. Given that all animals subjected to 10-min ischemic episodes showed ADC recovery with reperfusion, doubt is cast on whether it is possible to define a threshold value of the ADC below which brain tissue is irreversibly damaged. Finally, despite variability in the time constants of the ADC decay induced by ischemia, the ADC values at 10 min were very similar in all the animals. This suggests that when blood flow is diminished sufficiently to induce an ADC reduction, differences in perfusion affect the rapidity of the decrease but not the final asymptotic value reached.