Aritake K, Wakai S, Asano T, Takakura K
No To Shinkei. 1983 Oct;35(10):965-73.
Recent studies suggest that peroxidation of arachidonic acid (AA) accumulating during ischemic insult, may be related to the occurrence of post-ischemic brain damage. Since the influence of the increased brain content of AA remains unclear, the present study was undertaken to explore whether the intracerebral injection of AA is associated with the injury of the surrounding brain tissues such as brain edema. Rats received the intracerebral injection of 10 microliters of test solution (160 microgram of AA emulsified in 1% bovine serum albumin, BSA) or the same volume of BSA as the control. The measurement of specific gravity (SG) (74 rats) and the local CBF by H2 clearance technique (21 rats), and electron microscopical studies with tracers (Evans blue and horseradish peroxidase, HRP) (24 rats) were carried out. The effect of pretreatment with indomethacin (PI, 10 mg/kg) was evaluated in separate groups. AA transiently produced a significant decrease in SG and in 1CBF adjacent to the injection sites (p less than 0.01). The increased pinocytotic transportation, an accumulation of edema fluid containing HRP in extracellular space and endothelial injuries were observed only after AA injection. The above-mentioned falls in SG and in 1CBF, and the extravasation of HRP were inhibited by PI. The fact that PI prevented the edema formation, 1CBF change and the disturbance of blood-brain barrier induced by AA, indicates that peoxidation of AA through the arachidonate cascade is involved in the mechanism of brain edema formation.(ABSTRACT TRUNCATED AT 250 WORDS)
最近的研究表明,缺血性损伤期间积累的花生四烯酸(AA)过氧化作用可能与缺血后脑损伤的发生有关。由于脑内AA含量增加的影响尚不清楚,因此进行本研究以探讨脑内注射AA是否与周围脑组织损伤如脑水肿有关。给大鼠脑内注射10微升测试溶液(160微克AA乳化于1%牛血清白蛋白,BSA)或相同体积的BSA作为对照。进行了比重(SG)测量(74只大鼠)、用H2清除技术测量局部脑血流量(21只大鼠)以及用示踪剂(伊文思蓝和辣根过氧化物酶,HRP)进行电子显微镜研究(24只大鼠)。在单独的组中评估吲哚美辛预处理(PI,10毫克/千克)的效果。AA使注射部位附近的SG和局部脑血流量短暂显著降低(p<0.01)。仅在注射AA后观察到胞饮转运增加、细胞外空间中含有HRP的水肿液积聚以及内皮损伤。PI抑制了上述SG和局部脑血流量的下降以及HRP的外渗。PI预防了由AA诱导的水肿形成、局部脑血流量变化和血脑屏障破坏,这一事实表明通过花生四烯酸级联反应的AA过氧化作用参与了脑水肿形成机制。(摘要截短于250字)