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作 者:张惠光[1] 乔香兰[1] 王明礼[1] 邢凤友[2] 马青[2]
机构地区:[1]佳木斯医学院第一附属医院神经内科 [2]佳木斯医学院病生教研室
出 处:《中国病理生理杂志》1998年第1期50-53,共4页Chinese Journal of Pathophysiology
摘 要:目的和方法:选用热凝造成大脑中动脉阻断(MCAO)而致实验性大鼠脑局灶性缺血模型,观察汉防己甲素(tetrandrine,TET)对大鼠脑局灶性缺血的防治作用。结果:TET组用药七天,脑梗塞范围明显小于缺血组,缺血区脑组织Ca2+、Na+、过氧化脂质(LPO)、血浆血栓素B2(TXB2)明显低于缺血组,而超氧化物歧化酶(SOD)明显高于缺血组,6-酮-前列腺素F1α(6-ketoPGF1α)无显著改变,TXB2/6-酮(T/K)比值明显低于缺血组。结论:TET具有对大鼠MCAO局灶性脑缺血有效的防治作用,其机制可能与减少脑组织缺血区Ca2+、Na+、LPO含量,降低TXB2,使T/K比值趋于正常有关。AIM and METHOD: Using thermocautery,the middle cerebral artery(MCAO)of rats was occluded to produce an experimental cerebral infarction model.The protective and therapeutic effects of tetrandrine on cerebral infarction in rats were studied and its mechanism was discussed. RESULTS: At 7days after TET(50mg/kg,day)injection,the size of cerebral infarction in rats with TET group was reduced while compared with ischemic (I) group ( P <0 01),cerebral Ca 2+ ,Na +,LPO and TXB 2 lever were lower ( P <0 05) than I group,but SOD activity was increased,6-keto-PGF 1α levels had no difference,TXB 2/6 keto-PCF 1α (T/K)ratio were lower in TET group compared with ischemic group.CONCLUSIONS: TET could be used to protect and treat regional cerebral infarction from MCAO,the mechanism may be that TET can reduce cerebral Ca^2+ ,Na^+,LPO and plasma TXB 2 contents,and that TET made T/K radio close to normal. .
分 类 号:R743.330.5[医药卫生—神经病学与精神病学] R361[医药卫生—临床医学]
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