Pierpaoli C, Alger J R, Righini A, Mattiello J, Dickerson R, Des Pres D, Barnett A, Di Chiro G
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.
J Cereb Blood Flow Metab. 1996 Sep;16(5):892-905. doi: 10.1097/00004647-199609000-00013.
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 (tau +/- 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 approximately 15 min. No significant ADC changes were observed during hypoperfusion. Following cardiac arrest, the decay of ADC was more rapid in the thalamus (tau = 2.6 +/- 0.6 min) than in white matter (tau = 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.
尽管利用扩散加权磁共振成像对脑缺血进行了广泛研究,但迄今为止进行的大多数研究都没有足够的时间分辨率来跟踪超急性缺血时水表观扩散系数(ADC)的时间变化。利用扩散回波平面成像,我们在全脑缺血和再灌注的猫模型中以43秒的时间分辨率获得了ADC图(由8个b值的测量计算得出)。实施了不同的方案:10分钟低灌注、10分钟和22分钟缺血后再灌注以及心脏骤停。ADC值取自内囊白质和丘脑。由于皮质沟中脑脊液距离较近,皮质灰质测量结果被认为不可靠。闭塞后,丘脑的ADC在1.5 - 2.5分钟内降至其正常基线值的<2个标准差。这种衰减呈指数形式,时间常数(tau±标准差)为6.0±2.6分钟;缺血10分钟后未观察到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,在约15分钟内恢复到缺血前值。低灌注期间未观察到显著的ADC变化。心脏骤停后,丘脑ADC的衰减比白质更快(tau = 2.6±0.6分钟)(白质tau = 6.6±1.8分钟)。我们观察到心脏骤停后40分钟的ADC与缺血后10分钟的ADC相似。鉴于所有经历10分钟缺血发作的动物在再灌注后均显示ADC恢复,因此对于是否有可能定义一个ADC阈值,低于该阈值脑组织就会发生不可逆损伤产生了疑问。最后,尽管缺血诱导的ADC衰减时间常数存在差异,但所有动物在10分钟时的ADC值非常相似。这表明当血流充分减少以诱导ADC降低时,灌注差异会影响下降的速度,但不会影响最终达到的渐近值。