Association of the phosphatidylinositol signal pathway with prolonged myocardial ischemia  

作　　者：丁秀云[1] 王士雯[1] 高雪[1] 乐加昌[2] 李先锋[2] 

机构地区：[1]解放军总医院老年心血管病研究所,北京100853 [2]中国科学院生物物理研究所,北京100101

出　　处：《Chinese Medical Journal》2002年第3期367-370,共4页中华医学杂志（英文版）

基　　金：the National Great Foundamental Research Proiect (No．G2000057004) ; the National Nature Science Foundation of China(No．19890308)．

摘　　要：OBJECTIVE: To study the changes in activity of phosphatidylinositol 4 kinase (PI 4 kinase), phosphatidylinositol 4 phosphate 5 kinase (PIP 5 kinase) and protein kinase C (PKC) during myocardial ischemia and elucidate the relationship between phosphatidylinositol signal pathways and prolonged myocardial ischemia. METHODS: In vivo an ischemic rat model was used. Activity of PI 4 kinase, PIP 5 kinase and PKC were measured at different times in postischemic heart cells using isotope analysis. RESULTS: The activity of PI kinase, PIP kinase and PKC in the myocardium increased to peak at 1 hour postischemia, with activities 6.1, 3.0 and 4.0 fold over control levels, respectively. Their activities declined to normal levels with time. CONCLUSION: The phosphatidylinositol signal pathway is involved in prolonged myocardial ischemia, but its mechanism needs further study.目的　利用心肌缺血模型 ,研究磷酸肌醇 4激酶 (PI 4kinase)、磷酸肌醇磷酸激酶 (PIP 5Kinase)和蛋白酶C(PKC)在心肌缺血过程中的变化 ,以探讨磷酸肌醇信号系统在心肌缺血过程中调控的机理。方法　建立大鼠体内心肌缺血模型 ,利用同位素标记方法在蛋白水平上分别检测心肌组织缺血后不同时间 (缺血后 1、8、2 5、4 8小时 )磷酸肌醇 4 激酶 (PI4kinase)、磷酸肌醇磷酸激酶 (PIP 5Kinase)和蛋白酶C(PKC)活性的变化。结果　心肌组织中 ,磷酸肌醇 4 激酶、磷酸肌醇磷酸激酶和蛋白酶C的活性在心肌缺血后 1小时迅速达到最高值 ,分别为对照组活性的 6 1、3 0和 4 0倍 ,差异明显 ;随后酶活性水平开始下降 ,4 8小时已经接近对照组水平。结论　磷酸肌醇信号途径参与心肌缺血过程的调控 ,但其调控机理有待于进一步研究。

关 键 词：1-Phosphatidylinositol 4-Kinase Animals Male Myocardial Ischemia Phosphotransferases (Alcohol Group Acceptor) Protein Kinase C Random Allocation RATS Rats  Wistar Research Support  Non-U.S. Gov't Signal Transduction 

分 类 号：R540.2[医药卫生—心血管疾病]