大鼠基底节出血后血肿对锥体束的影响

Changes of pyramidal tract after intracerebral hemorrhage in a rat model

目的研究大鼠基底节出血后出血灶的变化和对锥体束的影响。方法选用体重250～300g的清洁级雄性sD大鼠72只，由中国医学科学院动物所提供，用随机数字表的方法随机分为正常对照组（8只）、假手术组（32只），Ⅳ型皎原酶-肝素诱导脑出血组（32只），其中假手术组和脑出血组再各分为4个亚组：1d组、3d组、7d组和14d组，每个亚组8只。使用Ⅳ型胶原酶一肝素诱导大鼠基底节出血，测量出血灶的血肿大小。采用HE染色、Luxolfastblue染色、Neurofilament免疫组化观察内囊后肢的病理改变，锥体束髓鞘的改变，锥体束NF染色的光密度值。所有数据使用SPSS13．0统计软件包进行分析，采用t检验、方差分析（ANOVA）和SNK—q检验。结果Ⅳ型胶原酶一肝素诱导的大鼠脑出血模型，1d组血肿体积最大．此后血肿逐渐吸收。3d组白质重度水肿，7d组白质胶质细胞大量增生。锥体束髓鞘损伤在脑出血1—3d逐渐加重，7d开始再生修复。锥体束轴突损伤从1d[（0．20±0．02）]到7d[（0．09±0．01）]持续加重，14d轴突光密度值[（0．10±0．02）]有所增加，但与7d无统计学差异（P〉0．05）。结论大鼠脑出血后锥体束的致伤原因除了血肿的直接破坏，还有脑水肿、炎症反应等各种复杂的继发病理生理改变的影响，脑出血早期若给予外科干预可能可以减轻锥体束的继发损伤。

Objective To study the change and pathological feature of hemorrhagic lesions and pyramidal tract after basal ganglia hemorrhage in a rat model. Methods Totally 72 male Sprague-Dawley rats of clean grade,weighting 250-300 g, provided by Animal Department of Chinese Academy of Medical Science,were divided into three groups randomly with numerical table method ： normal group （ n = 8 ）, the shame operation group（ n = 32）and the intracerebral hematoma group induced by Typeiv collagenase and heparin（n = 32）. Both the shame operation group and the intracerebral hematoma group were divided 4 subgroup：group 1 d, group 3 d, group 7 d and group 14 d, and each subgroup contained 8 rats. Type 1V collagenase and heparin were injected to the caudate nucleus of rats to induce intracerebral hemorrhage. The sizes of hematoma were determined in each group. HE stain, Luxol fast blue stain and neurofilament immunohistochemisty were performed to observe the pathological change of posterior limb of internal capsule, the change of myelin sheath of pyramidal tract and the optical density value of neurofilament immunohistochemisty stain of axons. The data was analyzed by SPSS 13.0 software package using t test, ANOVA and SNK-q test. Results Intracerebral hemorrhage model in rats was established by injection of type IV collagenase and heparin. The sizes of hematoma reached the maximum on day 1, and decreased gradually thereafter. It was found that in white substance severe edema occured on day 3, and glial ceils proliferated massively on day 7. Changes of myelin sheath of pyramidal tract aggravated on day 1 to 3 post cerebral hemorrhage, and remyelination initiated on day 7. Axons injury of pyramidal tract was aggravated continuously at 1 d [ （0. 20 ± 0. 02 ） ] to 7 d [ （0.09 ± 0. 01 ） ], and improved slightly with optical density value[ （0. 10 ±0. 02 ）] at 14 d, which had no statistic difference compared with that at 7 d （P 〉 0. 05 ）. Conclusions Injury of pyramidal tract after intracerebral hemorrhage in a rat model was caused by the direct damage of hemorrhage, and also by a secondary pathophysiological process full of many complex factors such as cerebra[ edema and inflammation. The surgical intervention performed in early period of intracerebral hemorrhage might reduce the tract＇s secondary injury.