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机构地区:[1]镇江医学院生化教研室 [2]贵州省老年医学研究所
出 处:《贵阳医学院学报》1991年第2期116-118,共3页Journal of Guiyang Medical College
摘 要:本研究采用阻断大鼠四条血管的全脑缺血模型,用酶联免疫吸附测定法观察下丘脑、海马、额叶大脑皮层和小脑中钙调蛋白(CaM)含量的变化。结果发现缺血30min后,除额叶大脑皮层外,上述脑区的CaM含量都明显下降;缺血30min再灌注6h后,CaM含量又进一步下降。提示在急性全脑缺血所致脑细胞损伤的发生发展过程中,脑组织中CaM含量的降低可能起着重要作用。In the rats anesthetized with hydrochloric acid ketamine, acute complete cerebral ischemia was produced by occluding the four arteries which supply the brain. 9 rats were killed after ischemia for 30 min and other 9 rats were hilled after reperfusion for 6h. The levels of calmodulin (CaM) in the hypothalamus, hippocampus, cerebral cortex and cerebellum were assayed by ELISA. As compared to the normal controls, the rats with ischemia showed a marked decline of the CaM level in all areas but the cerebral cortex (P<0.05 or p<0.01). In the rats with ischemia followed by reperfusion, the CaM levels presented a continuative decline trend in all cerebral areas, the CaM levels of the cerebral cortex and cerebellum being significantly different from that of the ischemia group (P<0.01). The authors discussed the possible action of the CaM in cerebral ischemic injury.
分 类 号:R743.310.2[医药卫生—神经病学与精神病学]
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