Photochemically induced cerebral infarction. II. Edema and blood-brain barrier disruption.
Photochemically induced cerebral infarction. II. Edema and blood-brain barrier disruption.
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DOI：
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发表时间：
1987
影响因子：
12.7
通讯作者：
W. Dietrich;R. Busto;B. Watson;P. Scheinberg;M. Ginsberg
中科院分区：
文献类型：
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作者：
W. Dietrich;R. Busto;B. Watson;P. Scheinberg;M. Ginsberg
在光化学诱导的小血管血栓形成导致梗死的大鼠模型中，记录了血脑屏障蛋白质、局部水和电解质含量的变化。辣根过氧化物酶（HRP）或伊文思蓝后立即给予2分钟的光化学敏化期。照射后5分钟，在照射区域内观察到多灶性过氧化物酶外渗部位。超微结构检查显示内皮细胞充满HRP，在某些情况下延伸到基底层和细胞外间隙。在15分钟时，蛋白质渗漏在照射区域内更明显，并且反应产物在远离照射部位的脑区域的蛛网膜下腔和血管周围空间内也很明显。广泛的染色表面上的照射半球是明显的大鼠灌注8小时后，伊文思蓝输注。水含量显着增加15分钟内照射区，但不是在远离这个网站的大脑区域。尽管血管源性水肿是该卒中模型的早期事件，但含水量的增加仅限于不可逆损伤部位。与此相反，蛋白示踪剂逃逸的微血管内的照射区广泛分布。这些发现暗示在该模型中组织损伤的发生中内皮屏障功能障碍。形态学证据的大分子的能力，从不断发展的梗死部位逃逸，并迁移到远离原发性微血管损伤的区域进行了讨论。
Alterations in the blood-brain barrier to proteins, and regional water and electrolyte content were documented in a rat model of photochemically induced small-vessel thrombosis leading to infarction. Horseradish peroxidase (HRP) or Evans blue was given immediately following a 2-min photochemical sensitization period. At 5 min following irradiation, multifocal sites of peroxidase extravasation were noted within the irradiated area. Ultrastructural examination revealed endothelial cells filled with HRP which in some cases extended into the basal lamina and extracellular spaces. At 15 min, protein leakage was more pronounced within the irradiated zone and reaction product was also apparent within the subarachnoid and perivascular spaces of brain regions remote from the site of irradiation. Widespread staining on the surface of the irradiated hemisphere was apparent in rats perfused 8 h following Evans blue infusion. Water content increased significantly by 15 min within the irradiated zone but not in brain regions remote from this site. Although vasogenic edema is an early event in this stroke model, increases in water content are restricted to the irreversibly damaged site. In contrast, protein tracer escaping from microvessels coursing within the irradiated zone was widely distributed. These findings implicate endothelial barrier dysfunction in the genesis of tissue injury in this model. Morphological evidence for the capability of macromolecules to escape from a site of evolving infarction and to migrate to distances remote from the area of primary microvascular damage is also discussed.