| Myocardial ischemia reperfusion injury(MIRI) is a very common clinic phenomenon .With the development of PTCA(percutaneous transluminal coronary angioplasty) and CABG(coronary artery bypass graft) et al , MIRI was more and more concerned by the people. Nearly,lots of scientific research personnel were engaged in preventing MIRI. Murry etc. firstly brought forward the concept of ischemic protectioning (IPC) in 1986.The heart possesses a remarkable ability to adapt to stress that makes it more resistant to injury.Subsequntly, IPC was found to be a biphasic phenomenon,with an early phase of protection that develops within minutes from the initial ischemic insult and lasts 2 to 3 hours and a late phase that becomes apparent 12 to 24 hours later and lasts 3 to 4 days.Unlike the early phase ,the late phase of ischemic PC protects not only against myocardial infarction but also against myocardial stunning.Because of this, and because of its sustained duration,considerable interesting has recently focused on the late phase and on its clinical relevance. Though preconditioning could induce myocardial protection, it is a wounded process and its potential dangers induced that it could not be used videly in clinic . So ,using drugs instead ischemic mimic IPC to protect myocardial reperfusion injury become the new interested focuse. At present ,few drugs were already used in PC and were proved possessing myocardial protection effects ,that include PNS,ligustrazine,low dose TNFα,IL-1β,allittidum etc.Experiments proved that those drugs all can induce myocardial delayed protective effects,and its mechanism is also related to the increased expression of HSP70.The protection showed in lowing the rates of ventricular arrhythmia , contracting myocardial infarct size, reducing myocardial stunning , decreasing energy metabolize et al. [key words]myocardial ischemic reperfusion injury ; heat shock protein ;preconditioning; immunohistochemistry；NF-κB. Objective to investigate whether there have delayed cardioprotection in ischemia reperfusion with fosinopril pretreatment in rats and explore the mechanism .Methods twenty-four Wistar rats were randomly divided into four groups ,namely, the control group(C group); fosinopril preconditioning group (Fos group);only ischemia reperfusion group(I/R) and PDTC +Fos group . All the rats were subjected to ischemia for 30 minutes followed by reperfusion for 2 hours,and observed the changes of the infarct size ; the score of ventricular arrhythmia and the damnification of myocardial cells of each group observed under the optical microscope ; immunohistochemical SABC method was used to observe the expression of HSP70 in myocardial tissue after preconditioning 24 hours. Result 1.among the four groups , myocardial infarct size were significantly decreased in Fos group than that in I/R group. The difference have statistical meaning(P<0.01) .The infarct range of PDTC +Fos group were larger than that of Fos group, the difference have statistical meaning(P<0.05).The infarct range of PDTC +Fos group were smaller than that of I/R group (P<0.05). 2. Fos group significantly decreased reperfusion ventricular arrhythmia than I/R ,the difference have statistical meaning(P<0.01) .The score of ventricular arrhythmia in Fos group is lower than that of PDTC +Fos group (P<0.01); The score of ventricular arrhythmia in PDTC+Fos group is lower than that of I/R group (P>0.05).The score of I/R group ,Fos group and PDTC+Fos group is higher than that of C group ,the difference have statistical meaning(P<0.01) .3.the damnification of myocardial cells of Fos group is lighter than that of I/R group and PDTC+Fos group observed under the optical microscope ,but it was more serious than that of C group ；the damnification of myocardial cells of PDTC+Fos group is lighter than that of I/R group .4.myocardial HSP70 mostly expressed at cytoplasm, and it was elevated significantly in Fos group compared with that in other three groups ,the difference have statistical mean...
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