Ohnishi T, Iwasaki H, Hayakawa T, Shapiro W R
Department of Neurosurgery, Osaka University Medical School, Japan.
Acta Neurochir Suppl (Wien). 1990;51:65-7. doi: 10.1007/978-3-7091-9115-6_22.
Free arachidonic acid was infused into normal rat brains and the effect of arachidonic acid on capillary permeability was investigated by measuring the regional uptake of 14C-aminoisobutyric acid with a quantitative autoradiographic method. Arachidonic acid increased capillary permeability in a dose-dependent manner up to 2 mM. A high dose of arachidonic acid (greater than 5 mM) produced a profound tissue destruction around the needle track and less increased capillary permeability than 2 mM arachidonic acid. Time-course study disclosed that arachidonic acid markedly increased capillary permeability within 2 hours after infusion, and continued to increase with time to 24 hours. The effect of 48 hours infusion was about a half of that at 24 hours, indicating that the effect of arachidonic acid was partially reversible. Pretreatment with dexamethasone significantly inhibited the arachidonic acid-induced increase in capillary permeability and the administration of actinomycin D 1 hour before the pretreatment with dexamethasone suppressed the inhibitory effect of dexamethasone. These results suggest that arachidonic acid, which is deposited in the extracellular space, increases brain capillary permeability by two different ways. One is the direct detergent effect of arachidonic acid, and the other is the effect of arachidonic acid that is released from the membrane by the activation of phospholipase A2.
将游离花生四烯酸注入正常大鼠脑内，采用定量放射自显影法通过测量¹⁴C -氨基异丁酸的局部摄取量，研究花生四烯酸对毛细血管通透性的影响。花生四烯酸以剂量依赖方式增加毛细血管通透性，直至2 mM。高剂量（大于5 mM）的花生四烯酸在针道周围产生严重的组织破坏，且与2 mM花生四烯酸相比，毛细血管通透性增加较少。时间进程研究显示，花生四烯酸在注入后2小时内显著增加毛细血管通透性，并随时间持续增加直至24小时。48小时注入的效果约为24小时时的一半，表明花生四烯酸的作用部分可逆。地塞米松预处理显著抑制花生四烯酸诱导的毛细血管通透性增加，且在用地塞米松预处理前1小时给予放线菌素D可抑制地塞米松的抑制作用。这些结果表明，沉积在细胞外空间的花生四烯酸通过两种不同方式增加脑毛细血管通透性。一种是花生四烯酸的直接去污剂作用，另一种是通过磷脂酶A2激活从膜释放的花生四烯酸的作用。
