丁基苯酞对全脑缺血大鼠的纹状体细胞外液嘌呤类代谢物含量的影响  

EFFECT OF DL-3-N-BUTYLPHTHALIDE(NBP)ON PUKINE METABOLITES IN STRIATUM EXTRACELLULAR FLUID IN FOUR-VESSEL OCCLUSION RATS

作　　者：胡盾[1] 黄新祥[1] 冯亦璞[1] 

机构地区：[1]中国医学科学院,中国协和医科大学药物研究所,镇江医学院

出　　处：《药学学报》1996年第1期13-17,共5页Acta Pharmaceutica Sinica

摘　　要：采用大鼠４动脉阻断的全脑缺血模型，用推挽式微灌流方法，用ＨＰＬＣ－ＵＶ检测缺血及重灌期纹状体灌流液中腺苷（Ａｄｅ）、肌苷（Ｉｎｏ）、次黄嘌呤（Ｈｙｐ）和黄嘌呤（Ｘａｎ）的含量。结果表明，ｉｐ丁基苯酞２０或４０ｍｇ·ｋｇ^(－１)均能显著降低大鼠全脑缺血纹状体细胞外液Ａｄｅ，Ｉｎｏ，Ｈｙｐ和Ｘａｎ的升高。但对假手术组动物则无影响。Ｈｙｐ和Ｘａｎ是产生氧自由基的底物。丁基苯酞这一抑制作用提示它对缺血性神经元的损伤有保护作用。The effects of NBP on concentrations of some purine metabolites in extracellular fluid of rat striatum during global ischemia and reperfusion were studied.Global ischemia wasproduced by the four vessel occlusion method,Push-pull cannula was implanted stereotaxically intothe striatum of rat and was perfused with Ringer’s solution at a flow rate of 2.5μl·min-1.Thelevel of adenosine(Ade),inosine(Ino),hypoxanthine(Hyp)and xanthine(Xan)in perfusates weremeasured with HPLC connected with a UV detector.The results indicate that the levels of ade,ino,hyp and xan were significantly increased(about 3～5times of initial value)during cerebral ischemiaand reperfusion,NBP at the dose of 2 0 or 40 mg·kg-1 given intra-peritoneally 20 min beforeischemia was shown to depress the increase of ade,ino,hyp and xan during ischemia and reperfusiondose dependently.But no change in the level of purine metabolites was found in sham operated rats。Ithas been known that harmful free radicals were produced when xan and uric acid were formed byxanthine oxidase during reperfusion,This might be important for the development of ischemic injuries。Our findings suggest that the effect of NBP might be beneficial for protection against post-ischemicneuronal damage。

关 键 词：丁基苯酞 微灌流 纹状体 嘌呤类代谢物 脑缺血 

分 类 号：R972[医药卫生—药品] R743.305[医药卫生—药学]