线粒体钙、钙调素、兴奋性氨基酸、丙二醛在脑缺血再灌注中变化的实验观察

Expermental research of MCa, CaM, EAA, MDA on ecrebral ischemic reperfusion damage

目的：观察脑缺血再灌注中线粒体钙（MitochondriaCaloium,MCa）、钙调素（Calmodulin,CaM）、兴奋性氨基酸（ExcitatoryAminoAcid,EAA）、丙二醛（Malondiadehyde,MDA）的动态变化,研究探索其变化时相,为阻抑其自稳平衡紊乱的发生提供科学的时间效应点。方法：采用大鼠全脑缺血再灌注模型（4VO）,测定假手术组、缺血30min再灌注1h、6h、12h组大脑皮层、海马组织MCa、CaM、EAA、MDA的含量。结果：缺血30min再灌注1h鼠大脑皮层、海马组织MCa、CaM、MDA含量显著升高，EAA含量显著降低，再灌注6h后，MCa、CaM继续升高，EAA、MDA回复到假手术组水平,当再灌注到12h时．MCa、CaM也相继回复到假手术组水平。结论：脑缺血再灌注早期（1h），Ca++、EAA、氧自由基自稳平衡紊乱发生，Ca++自稳平衡紊乱回复较EAA、氧自由基晚。

Objective: To study the change time point of MCa, CaM, EAA (glutamate,asparate),MDA on cerebral ischemic reperfusion damage. Methods: We observed the change of telenccphalon cor-tex, hippocampus MCa. CaM. EAA. MDA of the rat cerebral ischemia 30min reperfusion 1h, 6h. 12hand sham group (n = 8 ), the model of 4 - vessel occlusion was made. Results: The MCa, CaM. MDA con-tent significantly increased. the EAA 's decreased significantly on tschemia 30min reperfusion 1h. Reperfu-sion 6h,the EAA, MDA content came back to mormal level. but MCa .CaM content continually increascdsignificantly. Reperfusion 12h, MCa, CaM contcnt also rcturned to normal level.Conclusions: The abnormal balance of Ca+1, EAA, oxygen free radicals initiate carly,the abnormal balance of Ca++ rccovers later than the EAA and oxygen free radicals abnormal balance.