摘要
结扎兔双侧椎动脉和颈总动脉,导致急性脑缺血。缺血30min后重新开放双侧颈总动脉,使再灌注。脑缺血30min再灌注2h后,脑脊液中β—内啡肽免疫活性物质含量比缺血前增加1.01±0.52mg/L。icv苯环利定20μg/kg组,脑脊液中β—内啡肽免疫活性物质含量比缺血前增加0.36±0.32mg/L。icv苯环利定80μg/kg组,脑脊液中β—内啡肽免疫活性物质含量比缺血前下降0.19±0.44mg/L。提示苯环利定能抑制脑缺血后脑内β—内啡肽释放,减轻脑缺血性神经损伤。
Acute cerebral ischemia and reperfusion injury of rabbits was produced by permanently occluding the vertebral arteries and temporarily clamping the common carotid arteries for 30 min. Beta-endorphin immunoreactive substance ( ir beta-endorphin ) content were measured in cerebrospinal fluid at pre-ischemia and after ischemia and reperfusion stages. In control group, the content of ir beta-endorphin significantly increased (1.01±0.52 mg/L, P< 0.05). In phencyclidine 20μg/kg icv treated group, the content of ir beta-endorphin increased slightly ( 0.36 ± 0.32 mg/L) during ischemia and reperfusion, however in phencyclidine 80μg/kg icv treated group, the content or ir beta-endorphin decreased (0.19±0.44 mg/L), which was significant difference from control group ( P<0.05 ). These results indicate that phencyclidine may antagonize the centrally released beta-endorphin induced by acute cerebral ischemia and show benefical effects in cerebral ischemic damage.
出处
《中国药理学通报》
CAS
CSCD
北大核心
1992年第2期104-106,共3页
Chinese Pharmacological Bulletin
基金
高等学校博士学科点专项科研基金资助项目
关键词
Β内啡肽
脑脊液
脑缺血
苯环利定
Phencyclidine
Beta-Endorphin
Cerebral ischemia
Cerebrospinal fluid
Rabbits