摘要
用阻断四血管方法造成大鼠急性脑缺血再灌注损伤，缺血３０ｍｉｎ，再灌１ｈ，阿托品１ｍｇ／ｋｇ和２ｍｇ／ｋｇ静脉注射可阻止脑组织中超氧化物歧化酶（ＳＯＤ）活性降低，阻止脑组织和外周血中乳酸脱氢酶（ＬＤＨ）活性降低及过氧化脂质的升高（ＬＰＯ），抑制脑水肿形成，促进脑电活动的恢复，阿托品２ｍｇ／ｋｇ静脉注射也可以阻止外周血中ＳＯＤ活性降低，结果提示：阿托品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。
The
ligation of bilateral vertebral and common carotid arteries produced acutecerebral
ischemia-reperfusion injuries in rats. After 30 min ischemia followed 60 min
reperfu-sion,atropine(Atr)at the dose of 1 mg/kg and 2 mg/kg iv may suppress the reduction of
su-peroxide dismutase(SOD)activities in brain tissue and of lactic
dehydrogenase(LDH)activities and decrease the rise of lipid peroxides(LPO)both in brain tissue
and in blood,in-hibit brain edema formation and promote the recovery of EEG activities.The
reduction of su-peroxide dismutase(SOD)activities in blood was also suppressed by Atr at the
dose of 2mg/kg iv.The results suggested that Atr have protective effect on acute forebrain
ischemiaand reperfusion injuries in rats. The underlying mechanism is ascribed partially to the
anti-lipid peroxidation.
出处
《河南医学研究》
CAS
1995年第3期229-231,共3页
Henan Medical Research
关键词
阿托品
脑缺血
再灌注损伤
过氧化脂质
药理学
atropine,acute cerebral ischemia-reperfusion injury,anti-lipid
peroxidation
