Aarabi B, Long D M
J Neurosurg. 1979 Dec;51(6):779-84. doi: 10.3171/jns.1979.51.6.0779.
Brain edema was produced in cats by a standardized cortical freezing lesion. With a careful microsurgical tehnique, the injured cortex was removed as a single piece, either immediately after induction or at 2, 4, or 8 hours after lesion production. The injured brain was either discarded or replaced in its bed. Brain edema and the defect in the blood-brain barrier were assessed by determining percent dry weight, increase in volume of white matter, and spread of Evans' blue by planimetry. The results indicate that 1) if the lesion is removed immediately after production, formation of the expected vasogenic brain edema is completely abolished; 2) replacement of the frozen brain is unable to induce significant increase in permeability of the surrounding blood-brain barrier or a significant amount of brain edema; and 3) if the lesion is removed at 2, 4, or 8 hours with or without replacement, advancement of the edema front and increase in the amount of edema is stopped. It appears that an intact vascular bed is necessary for the extracellular fluid component of brain edema, and that no edemagenic factors exist within the injured brain in this model that influence either the production or propagation of the increased extracellular fluid volume.
通过标准化的皮质冷冻损伤在猫身上制造脑水肿。采用精细的显微外科技术,在损伤诱导后立即,或在损伤产生后2、4或8小时,将受伤的皮质作为一个整体切除。受伤的脑组织要么被丢弃,要么放回原位。通过测定干重百分比、白质体积增加以及用平面测量法测量伊文思蓝的扩散来评估脑水肿和血脑屏障的缺陷。结果表明:1)如果在损伤产生后立即切除损伤组织,预期的血管源性脑水肿的形成将被完全消除;2)将冷冻的脑组织放回原位不能诱导周围血脑屏障的通透性显著增加或大量脑水肿;3)如果在2、4或8小时切除损伤组织,无论是否放回原位,水肿前沿的进展和水肿量的增加都会停止。似乎完整的血管床对于脑水肿的细胞外液成分是必需的,并且在该模型中,受伤的脑组织内不存在影响细胞外液体积增加的产生或传播的致水肿因子。