Olah L, Wecker S, Hoehn M
Department of Experimental Neurology, Max-Planck-Institute for Neurological Research, Cologne, Germany.
J Cereb Blood Flow Metab. 2000 Oct;20(10):1474-82. doi: 10.1097/00004647-200010000-00009.
Recent investigations on transient focal cerebral ischemia suggested recovery of energy metabolism during early reperfusion, but followed by secondary energy failure. As disturbances of energy metabolism are reflected by changes of the apparent diffusion coefficient (ADC) of water, the aim of the current study was to follow the dynamics of the ADC during 1 hour of middle cerebral artery occlusion (MCAO) and 10 hours of reperfusion. The right MCA was occluded in male Wistar rats inside the magnet using a remotely controlled thread occlusion model. Diffusion-, perfusion-, and T2-weighted images were performed repetitively, and ADC, perfusion, and T2 maps were calculated and normalized to the respective preischemic value. The lesion volume at each time point was defined by ADC < 80% of control. At the end of 1-hour MCAO the hemispheric lesion volume was 22.3 +/- 9.0%; it decreased to 6.4 +/- 5.7% in the first 2 hours of reperfusion (P < 0.01), but then increased again, and by the end of 10 hours of reperfusion reached 17.3 +/- 9.3%. The mean relative ADC in the end ischemic lesion volume significantly improved within 2 hours of reperfusion (from 65.7 +/- 1.2% to 90.1 +/- 6.7% of control), but later declined and decreased to 75.4 +/- 7.3% of control by the end of the experiment. Pixels with secondary deterioration of ADC showed a continuous increase of T2 value during the first 2 hours of reperfusion in spite of ADC improvement, indicating improving cytotoxic, but generation of vasogenic edema during early reperfusion. A significant decrease of the perfusion level was not observed during 10 hours of recirculation. The authors conclude that the improvement of ADC in the early phase of reperfusion may be followed by secondary deterioration that was not caused by delayed hypoperfusion.
近期对短暂性局灶性脑缺血的研究表明，早期再灌注期间能量代谢有所恢复，但随后会出现继发性能量衰竭。由于能量代谢紊乱可通过水的表观扩散系数（ADC）变化反映出来，本研究的目的是观察大脑中动脉闭塞（MCAO）1小时及再灌注10小时期间ADC的动态变化。采用遥控线栓闭塞模型，在雄性Wistar大鼠磁体内闭塞右侧大脑中动脉。重复进行扩散加权、灌注加权和T2加权成像，并计算ADC图、灌注图和T2图，并将其归一化为各自的缺血前值。每个时间点的梗死体积定义为ADC < 对照值的80%。MCAO 1小时结束时，半球梗死体积为22.3±9.0%；再灌注前2小时降至6.4±5.7%（P < 0.01），但随后又增加，再灌注10小时结束时达到17.3±9.3%。最终缺血梗死体积内的平均相对ADC在再灌注2小时内显著改善（从对照值的65.7±1.2%提高到90.1±6.7%），但随后下降，实验结束时降至对照值的75.4±7.3%。尽管ADC有所改善，但ADC继发性恶化的像素在再灌注的前2小时内T2值持续增加，表明细胞毒性改善，但在早期再灌注期间出现了血管源性水肿。在再循环10小时期间未观察到灌注水平的显著下降。作者得出结论，再灌注早期ADC的改善之后可能会出现继发性恶化，这并非由延迟性低灌注引起。
