实验性心肌梗塞大鼠冠脉等组织纤溶因子表达的变化

通过观察大鼠实验性急性心肌梗塞（AMI）时，冠状动脉及周围心肌组织组织型纤溶酶原激活剂（t－PA），及其特异性抑制因子（PAI－1）基因表达及t－PA活性变化，从纤洛因子失衡方面探讨AMI发病机理，并研究缺血预处理调整纤溶功能的保护作用。结果表明，缺血和缺血再灌时组织t－PA活性均显著降低（P＜0．01），经预处理的缺血心肌t－PA活性有所升高（与缺血组相比P＜0．01）。AMI时t－PA、PAI－1表达均呈高水平，分别为对照组的1．19信和4．59倍而预处理组表达减弱。说明t－PA、PAI－1失衡参与AMI发展过程，缺血预处理对心肌的保护可能与纠正上述纤溶因子失衡有关。

Changes of Fibrinolytic Factors Expression of Coronary Arteries in Acute Myocardial Infarction

In present study, the changes of fibrinolytic factors activity and gene expression were invesigated incoronary artery tiussues in rats with AMI. The protective effect of ischemic preconditioning was also observed in this model. A ligature(5~0 silk )was placed around the left anterfor descending coronary artery close to its origin of each rat to reconstruct AMI animal model. Wistar rats were divided randomly into four groups (n =5);(J)Control (simulating the operation ); (2) Ischemia (ligaturing for 60min); (3) Reperfusion (ligaturing 60min, thenreperfusing for 20min); (4) Preconditioning (ligaturing 60min after twice 5 min tying up). The fibrinolytic activity and gene expression of coronary arteries and their periphery tissues were examined through spectrophotometric assay (ehromogenic substrate S2390),Northern blot and Dot blot respectively.The results showed that: (1) Tissue t-PA activity in ischemia and reperfusion was significantly lower than that in normal control (P<0.01 ). (2)Analysis by Northern blot and Dot blot revealed that t-PA and PAI-1mRNA expression in AMI rats were much higher than those in normal control,while PAI-1 expressed lower if The rats had been treated with ischemic preconditioning. These data suggested that unbalanced expression of t-PA and PAI-1 was involved in the development of AMI. Ischemic preconditioning may be effective to protect myocardium through correcting the imbalance of fibrinolytic factors.