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全脑缺血后PAF和细胞内钙离子的变化及相关机制研究
引用本文:张雄,阮旭中,王伟. 全脑缺血后PAF和细胞内钙离子的变化及相关机制研究[J]. 中风与神经疾病杂志, 2000, 17(6): 322-324
作者姓名:张雄  阮旭中  王伟
作者单位:同济医科大学附属同济医院临床神经医学研究中心,湖北武汉 430030
基金项目:本课题为国家自然科学基金重点资助项目(39870260)
摘    要:目的 探讨血小板活化因子(PAF)在缺血性脑损伤中的作用机制。方法 大鼠全脑缺血再灌注后,分别应用放免法和Fura-2/AM荧光法测定海马组织中PAF、突触体游离钙(「Ca^2+」i)浓度。结果 缺血20min后,PAF含量显著高于对照组,再灌注240min时已降至对照组水平,再灌注480min后出现迟发性升高。对应「Ca^2+」i值随所观察的再灌注时间延长而增加。Tetrandrine(钙拮抗剂)能明显降低再灌注480min时PAF和「Ca^2+」i水平。结论 全脑缺血再灌主后,PAF的异常代谢与「Ca^2+」i水平密切关联,协同参与了神经细胞损伤的发生及发展。

关 键 词:血小板化因子 脑缺血 钙离子 粉防已碱
文章编号:1003-2754(2000)06-0322-03
修稿时间:2000-06-22

Study of relationship between platelet-activating factor and synaptosomal cytosolic free calcium in rat hippocampus ischemia-reperfusion
ZHANG Xiong,RUAN Xu zhong,WANG Wei.. Study of relationship between platelet-activating factor and synaptosomal cytosolic free calcium in rat hippocampus ischemia-reperfusion[J]. Journal of Apoplexy and Nervous Diseases, 2000, 17(6): 322-324
Authors:ZHANG Xiong  RUAN Xu zhong  WANG Wei.
Abstract:Objective In order to study the action and significance of platelet activating factor(PAF) on the cerebral ischemia reperfusion damage, the PAF and synaptosomal cytosolic free calcium concentrations([Ca 2 ]i) in rat hippocampus were observed dynamically.Methods 48 mature Wistar rats were randomly divided into seven groups: Sham operated control group, simple ischemia group, 60 minute, 240 minute, 480 minute, 720 minute reperfusion groups and Tetrandrine treated group. With the 4 vessel occlusion model(4VO), the rats were suffered from ischemia for 20 minutes, then reperfusion was allowed for 60, 240, 480, 720 minutes before decapitation. Sham operated control rats were the same except for the clamping vessels. Radioimmunoassay and fluorescent probe Fura 2 of Ca 2 indicator were applied to determine the PAF and synaptosomal cytosolic free calcium concentrations in rat hippocampus respectively. Results The PAF levels of simple ischemia group were significantly higher than that of control group(P<0.01),but progressively returned to basal values following 240 minute reperfusion(P>0.05), in addition, 480 minutes reperfusion later ,the PAF concentrations appeard to be delayed elevation (P<0.01). Compared with the control group, the [Ca 2 ]i showed a progressive increase from 0 minute to 720 minutes after reperfusion. However, pretreatment with Tetrandrine significantly attenuated the increase of the PAF and [Ca 2 ]i levels at 480min reperfusion. Conclusion It was considered that PAF increases could be closely related to changes of [Ca 2 ]i, suggest the onset and progress of ischemic neuropathological damages.
Keywords:Platelet activating factor  Calcium  Cerebral ischemia`
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