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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。
Rabbit bilateral vertebral artery and common carotid artery ligation, resulting in acute cerebral ischemia. Reopen bilateral common carotid artery 30min after ischemia to reperfusion. Cerebral spinal fluid β-endorphin immunoreactive substances increased by 1.01 ± 0.52mg / L compared with that before ischemia after cerebral ischemia 30min reperfusion 2h. icv phencyclidine 20μg / kg group, β-endorphin in cerebrospinal fluid immunosuppressive substances increased by 0.36 ± 0.32mg / L than before ischemia. icv phencyclidine 80μg / kg group, the content of β-endorphin immunoreactive substance in cerebrospinal fluid was decreased by 0.19 ± 0.44mg / L compared with that before ischemia. Phenyclidine was found to inhibit the release of β-endorphin in the brain after cerebral ischemia and relieve cerebral ischemic nerve injury.