REGIONAL LEVELS OF FREE FATTY-ACIDS AND EVANS BLUE EXTRAVASATION AFTER EXPERIMENTAL BRAIN INJURY
REGIONAL LEVELS OF FREE FATTY-ACIDS AND EVANS BLUE EXTRAVASATION AFTER EXPERIMENTAL BRAIN INJURY
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DOI：
10.1089/neu.1994.11.405
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发表时间：
1994-08-01
影响因子：
4.2
通讯作者：
PRASAD, MR
中科院分区：
文献类型：
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作者：
DHILLON, HS;DONALDSON, D;PRASAD, MR
近年来建立的大鼠脑损伤控制性皮质冲击（CCI）模型为了解创伤性脑损伤病理生理的神经化学机制提供了一个很好的工具。在本研究中，大鼠遭受低等级严重程度的外侧CCI脑损伤。他们的大脑在受伤后的不同时间被原位冷冻，以测量游离脂肪酸的区域水平。损伤后30 min、2.5 h和24 h左皮质损伤部位组织总游离脂肪酸增加。在受伤动物中，硬脂酸和花生四烯酸的增加略大于棕榈酸和油酸的增加。损伤动物损伤后2.5 h和24 h邻近皮质总游离脂肪酸水平均显著升高（p < 0.05）。损伤后各时间点损伤动物相邻皮质仅硬脂酸和花生四烯酸显著升高（p < 0.05）。虽然在损伤部位附近的左侧海马中游离脂肪酸总量没有显著增加，但硬脂酸盐和花生四烯酸盐浓度在损伤后30 min和2.5 h升高（p < 0.05）。在脑损伤后30min和10h，损伤动物同侧皮质的Evans蓝外渗明显增加。这些结果表明，外侧脑损伤后同侧皮质膜磷脂降解和血脑屏障破坏。这些结果还表明，花生四烯酸及其代谢物可能在大鼠皮质撞击性脑损伤相关的血脑屏障破坏中起中介作用。
The recently developed controlled cortical-impact (CCI) model of brain injury in rats serves as an excellent tool to understand some of the neurochemical mechanisms mediating the pathophysiology of traumatic brain injury. In this study, rats were subjected to lateral CCI brain injury of low-grade severity. Their brains were frozen in situ at various times after injury to measure regional levels of free fatty acids. Tissue total free fatty acids at the injury site within the left cortex were increased at 30 min, 2.5 h, and 24 h postinjury. In injured animals, increases in stearic and arachidonic acids were slightly greater than those in palmitic and oleic acids. The levels of total free fatty acids in the cortex adjacent to the injury site were also increased in injured animals at 2.5 h and 24 h after injury (p < 0.05). Only stearic and arachidonic acids were observed to be significantly increased (p < 0.05) in the adjacent cortex of injured animals at all times after injury. Although no significant increases in total free fatty acids were observed in the left hippocampus adjacent to the injury site, stearate and arachidonate concentrations were increased at 30 min and 2.5 h after injury (p < 0.05). Extravasation of Evans blue was found to be significantly increased in the ipsilateral cortex of injured animals at 30 min and 10 h after brain injury. These results indicate the degradation of membrane phospholipids and blood-brain barrier breakdown in the ipsilateral cortex after lateral CCI brain injury. These results also suggest that arachidonic acid and its metabolites may play a role as a mediator in the blood-brain barrier breakdown associated with cortical impact brain injury in rats.