摘要：

目的 探讨缺血性卒中大鼠梗死灶中心和周围白质纤维束损伤情况。 方法 共25 只Sprague-Dawley 大鼠随机分为对照组（10 只）和大脑中动脉闭塞组（MCAO 组，15 只），其中MCAO 组以线拴法制备大脑中动脉闭塞模型。两组大鼠分别于模型制备后3 h、6 h、1 d、2 d、3 d、4 d 和7 d，采用高场强（7.0T）扩散张量成像（DTI）和扩散张量纤维束示踪成像（DTT），于梗死侧皮质、皮质下和胼胝体选择兴趣区并计算部分各向异性（FA）值、平均扩散率（MD）值、轴向扩散系数（λ║）值和径向扩散系数（λ┴）值，以及于内囊区选择兴趣区并计数纤维数目（NT）值。 结果 两组大鼠不同时间点梗死侧皮质、皮质下和胼胝体FA 值（均P = 0.000）、MD 值（均P = 0.000）、λ║值（均P = 0.000）和λ┴值（均P = 0.000）差异均有统计学意义，MCAO 组梗死侧皮质、皮质下和胼胝体FA 值于超急性期（≤ 6 h）缓慢升高（均P = 0.000）、急性期（6 小时至3 天）明显下降（均P = 0.000）、亚急性期（3 天至8 周）趋于稳定，MD 值、λ║值和λ┴值均于急性期明显升高（均P = 0.000），亚急性期趋于稳定；对照组与MCAO 组大鼠梗死侧皮质、皮质下和胼胝体FA 值（P = 0.003，0.000，0.000），皮质下MD 值（P = 0.013），皮质下和胼胝体λ║值（P = 0.012，0.001）和λ┴值（P = 0.001，0.036）差异有统计学意义。两组大鼠不同时间点梗死侧NT 值差异有统计学意义（P = 0.000），MCAO 组梗死侧NT 值于超急性期缓慢下降（P = 0.032）、急性期明显下降（均P = 0.000）、亚急性期趋于稳定；MCAO 组大鼠各时间点梗死侧NT 值低于对照组（P = 0.000）。DTT 显示，MCAO 组大鼠梗死侧白质纤维束走行迂曲，部分离断，尤其模型制备1 d 后即可见梗死侧受损纤维趋于围绕病灶边缘。 结论 缺血性卒中超急性期至急性期，神经损伤持续存在，至亚急性期出现神经纤维重塑。DTT 显示梗死侧受损纤维趋于围绕病灶边缘，提示受损纤维包绕病灶的保护作用。

关键词: 动脉闭塞性疾病, 大脑中动脉, 磁共振成像, 疾病模型, 动物

Abstract:

Objective  To evaluate the damage of white matter fiber tracts in the center and periphery of infarcts in the model rats of ischemic stroke.  Methods  A total of 25 Sprague-Dawley (SD) rats were randomly divided into control group (N = 10) and middle cerebral artery occlusion (MCAO) group (N = 15). MCAO model was established by occluding with suture. At 3 h, 6 h, 1 d, 2 d, 3 d, 4 d and 7 d after model establishment, perform diffusion tensor imaging (DTI) and diffusion tensor tractography (DTT) at high-field 7.0T MRI, choose cortex, subcortex and corpus callosum of infarct side as regions of interest (ROIs) and calculate the values of fractional anisotropy (FA), mean diffusion coefficient (MD), radial diffusivity (λ║) and axial diffusivity (λ┴), choose internal capsule as ROI and calculate number of tracts (NT).  Results  At different time points, FA value (P = 0.000, for all), MD value (P = 0.000, for all), λ║ value (P = 0.000, for all) and λ┴ value (P = 0.000, for all) in the cortex, subcortex and corpus callosum ofinfarct side had significant difference between 2 groups. As time extended, in MCAO group FA value in cortex, subcortex and corpus callosum of infarct side was slowly increased in superacute phase (≤ 6 h; P = 0.000, for all), obviously decreased in acute phase (6 h to 3 d; P= 0.000, for all) and kept stable in subacute phase (3 d to 8 weeks). MD value, λ║ value and λ┴ value were obviously increased in acute phase (P = 0.000, for all) and kept stable in subacute phase. FA value in cortex, subcortex and corpus callosum of infarct side (P = 0.003, 0.000, 0.000), MD value in subcortex (P = 0.013), λ║ (P = 0.012, 0.001) and λ┴ (P = 0.001, 0.036) values in subcortex and corpus callosum had significant differences between 2 groups. At different time points, NT value of infarct side had significant difference between 2 groups (P = 0.000). As time extended, NT value of infarct side in MCAO group was slowly decreased in superacute phase (P = 0.032), obviously decreased in acute phase (P = 0.000, for all) and kept stable in subacute phase. Compared to control group, NT value of infarct side in MCAO group was significantly lower at each time point (P = 0.000). DTT showed the white matter fiber tracts of infarct side in MCAO group were twisted and fractured. The damaged fibers tended to be around the edge of the lesion 1 d after MCAO model establishment.  Conclusions  At the superacute phase to acute phase after ischemic stroke, nerve damage persisted until neural remodeling appeared in the subacute phase. DTT observed the damaged fibers tended to be around the edge of the lesion, suggesting the protective effect of damaged fibers surrounding the lesion.

Key words: Arterial occlusive diseases, Middle cerebral artery, Magnetic resonance imaging, Disease models, animal