苯海索对大鼠急性前脑缺血再灌注损伤的保护  

Protection of trihexpyphenidyl against acute forebrain ischemia reperfusion injury in rats

作　　者：胡香杰[1] 吕爱刚[1] 贾丹辉[1] 张贵 卿可君 

机构地区：[1]河南医科大学药理学教研室

出　　处：《中国药理学通报》1997年第4期364-366,共3页Chinese Pharmacological Bulletin

基　　金：河南省教委自然基金

摘　　要：目的：研究苯海索（ｔｒｉｈｅｘｙｐｈｅｎｉｄｙｌ，ＴＨＰ）对大鼠急性前脑缺血再灌注损伤的保护作用。方法：用阻断四血管法造成急性前脑缺血再灌注损伤。ＴＨＰ１．５ｍｇ·ｋｇ－１或３ｍｇ·ｋｇ－１在缺血前５ｍｉｎ，再灌前和再灌注３０ｍｉｎ分３次静脉注射。结果：ＴＨＰ可剂量依赖性阻止脑组织和红细胞中超氧化物歧化酶活力下降及脑组织中乳酸脱氢酶（ＬＤＨ）活力下降，阻止外周血中ＬＤＨ活力增加和过氧化脂质含量增加，并促进脑电活动恢复和抑制脑水肿形成。结论：ＴＨＰ对大鼠急性前脑缺血再灌注损伤具有保护作用，其机制与抗脂质过氧化有关。AIM: To study the protective effect of trihexyphenidyl (THP) on acute forebrain ischemia reperfusion injury in rats. METHODS: Acute forebrain ischemia reperfusion injury was produced by permanent occlusion of the vertebral arteries and followed by temporary clamping of bilateral common carotid arteries. THP 3 mg·kg -1 or 1 5 mg·kg -1 was injected intravenously by 5 min before ischemia, 5 min before reperfusion, and 30 min after reperfusion. RESULTS: THP dose dependently suppressed the reduction of superoxide dismutase (SOD) activities in brain tissue and erythrocyte and of lactic dehydrogenase (LDH) activities in brain tissue. THP also decresed the rise of LDH activities in blood and of LPO contents both in brain tissue and in blood. The recovery of EEG activities was promoted and brain edema formation was inhibied. CONCLUSIONS: THP had protective effect on acute forebrain ischemia and reperfusion injuries in rats. The underlying mechenism is ascribed partially to the anti lipid peroxidation.

关 键 词：苯海索 脑缺血 再灌注损伤 抗胆碱药 

分 类 号：R971.91[医药卫生—药品] R743.310.5[医药卫生—药学]