Dhillon H S, Donaldson D, Dempsey R J, Prasad M R
Department of Surgery, University of Kentucky Medical Center, Lexington.
J Neurotrauma. 1994 Aug;11(4):405-15. doi: 10.1089/neu.1994.11.405.
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.
最近开发的大鼠脑损伤控制皮质撞击（CCI）模型是了解介导创伤性脑损伤病理生理学的一些神经化学机制的优秀工具。在本研究中，对大鼠进行轻度严重程度的侧方CCI脑损伤。在损伤后的不同时间将它们的大脑原位冷冻，以测量游离脂肪酸的区域水平。损伤后30分钟、2.5小时和24小时，左皮质损伤部位的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。在受伤动物中，损伤后2.5小时和24小时，损伤部位相邻皮质中的总游离脂肪酸水平也升高（p<0.05）。在受伤动物的相邻皮质中，仅在损伤后的所有时间观察到硬脂酸和花生四烯酸显著增加（p<0.05）。虽然在损伤部位相邻的左海马中未观察到总游离脂肪酸的显著增加，但硬脂酸盐和花生四烯酸盐浓度在损伤后30分钟和2.5小时增加（p<0.05）。发现在脑损伤后30分钟和10小时，受伤动物同侧皮质中的伊文思蓝外渗显著增加。这些结果表明侧方CCI脑损伤后同侧皮质中膜磷脂的降解和血脑屏障的破坏。这些结果还表明，花生四烯酸及其代谢产物可能在大鼠皮质撞击性脑损伤相关的血脑屏障破坏中作为介质发挥作用。
