卡托普利对电解灌流液所致兔离体脑基底动脉痉挛的保护作用  

Protective effect of captopril on electrolyzed perfusion solution induced vasospasm of isolated basilar artery

作　　者：陈剑雄[1] 廖端芳[1] 余麟 肖观莲 朱炳阳 唐小卿 

机构地区：[1]衡阳医学院药理教研室

出　　处：《中国药理学与毒理学杂志》1995年第1期44-46,共3页Chinese Journal of Pharmacology and Toxicology

基　　金：国家自然科学基金

摘　　要：１０ｍＡ直流电电解Ｋｒｅｂｓ液１ｍｉｎ引起兔基底动脉收缩，灌注压明显增高，血管壁组织丙二醛含量升高及兔胸主动脉，脑基底动脉内皮舒张因子（ＥＤＲＦ）释放量明显减少，卡托普利（Ｃａｐ）２５，５０，１００ｕｍｏｌ·Ｌ￣（－１）可浓度依赖性地抑制电解产生自由基诱发脑血管收缩作用，Ｃａｐ１００ｐｍｏｌ·Ｌ￣（－１）与吲哚美辛合用可完全取消Ｃａｐ的作用，此外Ｃａｐ１００ｕｍｏｌ·Ｌ￣（－１）还具有明显抑制血管壁丙二醛生成及保护内皮细胞释放ＥＤＲＦ的作用，提示Ｃａｐ对外源性氧自由基损伤脑血管保护作用可能由前列环素和ＥＤＲＰ共同中介。The perfusion pressure andmalonyldialdehyde(MDA) content of isolated rabbitbasilar arteries were increased significantly after ele-ctrolyzed Krebs perfusion solution(constant current.10 mA, 1 min),meanwhile release of endothelium de-rived relaxing factor(EDRF) in isolated rabbitthcracic aorta and basilar arteries decreased. Captopril(Cap) 25,50, 100 umol·L￣(-1)pretreatment resulted inaconcentration dependent decrease in constriction re-sponse of basilar arteries caused by electrolysis free rad-icals, and a combination of Cap 100 pmol· L￣(-1) andhdometacin 5 umol·L￣(-1)almost abolished the con-striction Results also showed that production ofMDA was decreased and release of EDRF increasedby Cap at 100 umol·L￣(-1).These data indicated thatprotective effect of Cap against electrolysis induced cer-ebral vascular damage is mediated by the combined ef-fect of the prostacvclin and EDRF.

关 键 词：血管舒张药 卡托普利 基底动脉 兔 药理 

分 类 号：R972.4[医药卫生—药品]