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 the Rabbits

建立兔大脑中动脉阻断(MCAO)局灶脑缺血实验模型。通过不连续梯度超速离心脑微血管(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的Na^+,K^+-ATP酶活性则随时相递降,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 microvesscls (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 cerebral 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 decreases in the enzyme activity. These changes are presumed to occur due to stimulated active transport of sodium from blood to brain across the brain capillaries. On the contrary,a decrease in SPM Na+,K+-ATPase activity was observed in all ischemic groups. It is suggested that the changes of activity of Na+,K+-ATPase may participate in the pathogenesis of ischemic biain edema.