DEVELOPMENT OF TISSUE-DAMAGE, INFLAMMATION AND RESOLUTION FOLLOWING STROKE - AN IMMUNOHISTOCHEMICAL AND QUANTITATIVE PLANIMETRIC STUDY
DEVELOPMENT OF TISSUE-DAMAGE, INFLAMMATION AND RESOLUTION FOLLOWING STROKE - AN IMMUNOHISTOCHEMICAL AND QUANTITATIVE PLANIMETRIC STUDY
复制标题
DOI：
10.1016/0361-9230(93)90124-t
复制
发表时间：
1993-01-01
影响因子：
3.8
通讯作者：
BARONE, FC
中科院分区：
文献类型：
--
作者：
CLARK, RK;LEE, EV;BARONE, FC
通过定量面积测量和组织学/免疫组织化学技术研究了大脑中动脉（MCAO）闭塞所产生的病变的发展和解决方案。在自发性高血压大鼠（SHR）中进行的MCAO最初（1-3天）产生大的、一致的大脑皮质梗死和同侧半球大小的增加（即，肿胀），通过在2，3，5-氯化三苯基四唑（TTC）染色的大体组织切片上进行面积测定来定量。这些最初的变化相关性以及从2小时至3天使用苏木精和伊红染色的组织切片和免疫组织化学技术，包括确定的变化：进行性发展的皮质区泛坏死，中性粒细胞浸润到梗死组织，和星形胶质细胞的激活。在最初的2天后MCAO，胶质细胞酸性蛋白免疫反应细胞的数量增加，变得更大，更强的荧光皮质梗死内侧。第5 ~ 15天，梗死灶和同侧大脑半球均缩小。这些变化与大量巨噬细胞的存在和病变沿着内侧边缘的空化有关。在此期间，沿着梗死表面形成疏松的结缔组织基质。该结缔组织含有成纤维细胞、层粘连蛋白和胶原免疫反应性细胞外基质、指示新血管形成的毛细血管芽和丰富的巨噬细胞。到最终时间点（30天），在大体或组织学组织切片中不再检测到坏死组织，炎症浸润已消退，并去除结缔组织。本研究首次详细描述了局灶性缺血后的细胞/组织变化，并在整个脑缺血性损伤的发展和解决过程中提供了定量平面图和组织学/免疫组织化学信息的相关性。基于这些数据，细胞/组织事件的四阶段组织矩阵（即，神经元死亡、炎症、组织和消退），其定义了在永久性局灶性卒中中发生的通过脑愈合的梗死的演变。
Development and resolution of the lesion produced by occlusion of the middle cerebral artery (MCAO) was studied through quantitative planimetry and histologic/immunohistochemical techniques. MCAO, performed in spontaneously hypertensive rats (SHR), initially (1-3 days) produced large, consistent cerebral cortical infarctions and an increase in ipsilateral hemispheric size (i.e., swelling) quantitated by planimetry on 2,3,5-triphenyltetrazolium chloride (TTC)-stained gross tissue sections. These initial changes correlated well with changes identified from 2 h to 3 days using hematoxylin and eosin stained histologic tissue sections and immunohistochemical techniques including: the progressive development of a cortical area of pan necrosis, infiltration of neutrophils into infarcted tissues, and activation of astroglia. During the initial 2 days following MCAO, glial fibrillary acidic protein immunoreactive cells increased in number and became larger and more intensely fluorescent medial to the cortical infarct. At 5 to 15 days, both the infarct and the ipsilateral hemisphere decreased in size. These changes correlated with the presence of abundant macrophages, and cavitation of the lesion along its medial border. Also during this period, a loose connective tissue matrix formed along the superficial aspect of the infarct. This connective tissue contained fibroblasts, extracellular matrix immunoreactive for laminin and collagen, capillary buds indicating neovascularization, and abundant macrophages. By the final timepoint (30 days), necrotic tissue could no longer be detected in either gross or histologic tissue sections, the inflammatory infiltrate had resolved, and the connective tissue was removed. This study represents the first detailed description of the cellular/tissue changes following focal ischemia with a correlation of quantitative planimetric and histologic/immunohistochemical information provided throughout the development and resolution of cerebral ischemic damage. Based on these data, a four-stage organizational matrix of cellular/tissue events (i.e., neuronal death, inflammation, organization, and resolution) is presented that defines the evolution of infarction through cerebral healing that occurs in permanent focal stroke.