摘要目的　利用心肌缺血模型,研究磷酸肌醇4激酶（PI 4 kinase）、磷酸肌醇磷酸激酶（PIP 5 Kinase）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、25、48小时）磷酸肌醇4-激酶（PI 4 kinase）、磷酸肌醇磷酸激酶（PIP 5 Kinase）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,48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.

abstractsObjective 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.