摘要
目的：运用脑缺血再灌注模型，探索血小板活化因子及自由基在缺血性脑损伤中的地位及意义。方法：分别应用放免法及TBA法测定大鼠海马组织中PAF与LPO含量。结果：缺血20min后再灌注0min组及60min组PAF含量均显著高于假手术对照组，而再灌注240min组与假手术对照组比较已无显著差异。相应LPO含量早期随再灌注时间延长逐渐升高。结论：PAF可能主要参与脑缺血再灌注缺血期的病理损伤机制；而自由基的脂质过氧化作用增强发生在再灌注期。
: In order to study the action and significance of platelet-activating factor (PAF)andLipid peroxidex(LPO) on the cerebral ischemic damage,the levels in rat hipppocampus were observed dynamically.Methods: 26 mature Wistar rats were randomly divided into four groups: Sham-operated control group, O-minute,6o-minute and 240-minute reperfusion groups. With the 4-vessel occlusion (4VO )model, the rats were suffered fromischemia for 20 minutes, the reperfusion was allowed for 0. 60' 240 minutes before decapitation. Sham-operatedcontrol rats were the same except for the clamping vessels. Radioimmunoassay and thiobarbituric acid reaction wereapplied to measure tlle PAF and LPO concentrations of rat hippocampus recpectively. Results: The PAFconcentrations of O-minute reperfusion group were significantly higher then those of the control group (P<0. 01),but the PAF levels progressively returned to basal values following 240 minute reperfusion. Compared with thecontrol group, the LPO concentrations of O-minute reperfusion group were no significant difference (P> 0. 05),whereas the levels of 60-minute and 240-minute reperfusion groups showed a significant increase (P < 0. 01 ).Conclusion :The results suggested that PAF was involved in the early stages of the cerebral ischemia, especially insimple ischemic period , while the lipid hyperperoxidation might only occure in the reperfusion stage.[
出处
《卒中与神经疾病》
1999年第4期216-218,共3页
Stroke and Nervous Diseases
关键词
血小板活化因子
脂质过氧化
脑缺血
Platelet-activating factor Lip1d peroxidation Cerebral ischemia
