摘要
本文以蒙古沙土鼠双侧颈总动脉结扎造成脑缺血模型，研究了脑缺血和再灌注时大脑Ｃａ￣２＋／ＣａＭＰＫⅡ活性变化及苄丙咯对其活性的影响，实验结果：（１）Ｃａ￣２＋／ＣａＭＰＫⅡ活性随脑缺血时间的延长而逐渐降低，脑缺血１０分钟，酶活性显著低于正常组（Ｐ＜０．０１）；（２）脑缺血１０分钟再灌注２０分钟，酶活性部分恢复，与缺血１０分钟组相比，酶活性有明显上升（Ｐ＜０．０１），但缺血２０分钟再灌注，其活性不再恢复；（３）缺血前２０分钟腹腔注射苄丙咯，在缺血１０分钟时酶活性明显高于对照组（Ｐ＜０．０ｌ）。结果提示Ｃａ￣２＋／ＣａＭＰＫⅡ活性对缺血非常敏感；苄丙咯对该酶活性有一定保护作用。
The acute cerebral ischemia was formed by ligation of both common corotidarteries of the Mongolian gerbils. The changes of Ca￣2+/CaM PKⅡactivity from 40000gsupernatant of cortex during acute cerebral ischemia and reperfusion,and effect of bepridilon the enzyme activity were investigated.The results showed:(1) Ca￣2+/CaM PKⅡ activitydecreased progressively while the ischemic time prolonged.After l0 min ischemia, theenzyme activity in ischemic group was decreased more than that of normal group( P<0. 01 ); ( 2)in 20 min of reperfusion(after 10 min ischemia), the enzyme activity partia lly recovered and was much more increased compared with the enzyme activity of 10 minischemia group(P<0.01), but no recovery of the enzyme activity was shown duringreperfusion after 20 min ischemia ;(3 )after ap. of bepridil 20 min, the enzyme activityin 10 min ischemia group was increased more than that of control group (P<0.01). Theseresults suggested that Ca￣2+/CaM PKⅡ activity may be susceptible to cerebral ischemiaand bepridil may have protective effect to the enzyme activity.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1994年第2期139-142,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
