Masuda Y, Ochi Y, Ochi Y, Karasawa T, Hatano N, Kadokawa T, Okegawa T
Eur J Pharmacol. 1986 Apr 29;123(3):335-44. doi: 10.1016/0014-2999(86)90706-5.
Protective effects of OP-2507 [15-cis-(4-propylcyclohexyl)-16,17,18,19,20-pentanor-9-deoxy -9 alpha, 6-nitrilo-PGF1 methyl ester] against cerebral anoxia and edema were investigated in a variety of experimental models in mice and rats. OP-2507 given s.c. or p.o. led to a consistent and dose-dependent prolongation of survival time against cerebral anoxia in hypobaric and normobaric hypoxia, KCN-induced anoxia and decapitation-induced gasping. Furthermore, treatment with 0.03-0.1 mg/kg s.c. or 0.3 mg/kg p.o. of OP-2507 was found to be effective against the changes of cerebral energy metabolites and cyclic nucleotides in hypoxic brain. In brain ischemia induced by bilateral ligation of common carotid arteries of rats, a reduction in specific gravity of cortex and an increase in water content of brain were observed, in accordance with changes of cerebral energy metabolites. These edematous and biochemical changes were prevented by the treatment with 0.01-0.03 mg/kg s.c. of OP-2507. These results indicate a potential usefulness of OP-2507 in protecting the brain from oxygen insufficiency resulting from cerebral ischemia.
在小鼠和大鼠的多种实验模型中，研究了OP-2507[15-顺式-(4-丙基环己基)-16,17,18,19,20-五降-9-脱氧-9α,6-腈基-PGF1甲酯]对脑缺氧和脑水肿的保护作用。皮下或口服给予OP-2507可使小鼠在低压和常压缺氧、氰化钾诱导的缺氧及断头诱导的喘息等脑缺氧模型中的存活时间持续且剂量依赖性地延长。此外，发现皮下注射0.03 - 0.1mg/kg或口服0.3mg/kg的OP-2507可有效对抗缺氧脑中脑能量代谢物和环核苷酸的变化。在大鼠双侧颈总动脉结扎诱导的脑缺血中，观察到皮层比重降低和脑含水量增加，这与脑能量代谢物的变化一致。皮下注射0.01 - 0.03mg/kg的OP-2507可预防这些水肿和生化变化。这些结果表明OP-2507在保护大脑免受脑缺血导致的氧供应不足方面具有潜在用途。
