兔脑缺血后脑微血管和突触膜Na^+,K^+—ATP酶活性变化  

Changes in the activities of CMV,SPM Na^+,K^+-ATPase following MCAO model brain ischemia in thd rabbits

作　　者：张天锡[1] 卞留贯[1] 赵卫国[1] 

机构地区：[1]上海第二医科大学瑞金医院神经外科,200025

出　　处：《中风与神经疾病杂志》1994年第2期65-67,共3页Journal of Apoplexy and Nervous Diseases

基　　金：卫生部八五攻关项目资助

摘　　要：建立兔MCAO局灶脑块血实验模型。通过不连续梯度超迷离心分离脑微血管(CMV)和突触膜(SPM),用生化法分别测其Na^+,K^+-ATP酶活性。结果发现CMV Na^+,K^+-ATP酶活性在MCAO后先升后降,而SPM Na^+,K^+-ATP酶活性别随时相递降,且两者与脑水含量变化均有密切关系。提示CMV和SPM Na^+,K^+-ATP酶活性变化参与了脑缺血后早期脑水肿的发生发展。Changes in the activities of cerebral microvessels (CMV),synaptic plasma membranes (SPM) Na+,K+-ATPase and in the water, sodium levels in the ischemic brain were investigated in rabbits 2,4 and 24h following occlusion of middle cereral artery (MCAO) and in sham-occluded control. An increase in CMV Na+ ,K+ -ATPase activity was observed in 2h and 4h groups with a subsequent decrease in the enzyme activity. These changes are presumed to occur because of acumulated active transport of sodium from blood to brain across the brain capillaries. Oppositely, a decrease in SPM Na+ < K+ - ATPase activity was observed in all ischemic groups. We suggested that the changes of activity of Na+ ,K+ -ATPase may participate in the pathogenesis of ischemicbrain edema.

关 键 词：脑缺血 微血管 突触膜 腺苷三磷酸 

分 类 号：R743.310.2[医药卫生—神经病学与精神病学]