心脏缺血再灌注（Ischemia/ reperfusion，I/R）损伤是影响心肌梗塞治疗及预后的重要因素。我们的前期临床研究发现餐后发生心肌梗塞的病人预后优于餐前，而血浆胃泌素在餐后也有显著升高，并且在进食后0.5小时左右出现峰值，提示胃泌素可能在心脏I/R损伤中发挥保护作用。我们预实验发现胃泌素可以抑制心肌凋亡，减轻心脏I/R损伤。再灌注损伤救援激酶(reperfusion injury salvage kinase pathway, RISK) 途径在器官的I/R损伤的保护机制中扮演着重要的作用，我们通过预实验筛选发现胃泌素可以激活I/R心脏中的RISK途径的重要分子之一Akt。由此我们提出假设“胃泌素激活下游RISK通路抑制细胞凋亡，发挥对心脏I/R损伤的保护作用”。因此，本实验用离体和在体心脏缺血再灌注模型以及细胞缺氧复氧模型进行研究，明确胃泌素对心脏I/R损伤的保护作用及机制，

Cardiac ischemia-reperfusion（I/R) injury is an important factor affecting the treatment and prognosis of myocardial infarction. Our previous study found that the prognosis of postprandial myocardial infarction was superior than that of preprandial and plasma gastrin increased to the peak thirty minutes after the meal, suggesting that gastrin may play a protective role in cardiac I/R injury. Our preliminary experiments also found that gastrin could inhibit cardiomyocytes apoptosis and reduce cardiac I/R damage area. The reperfusion injury salvage kinase (RISK) pathway plays an important role in the protection of I/R injury. Our preliminary experiment discovered that gastrin could activate Akt , one of the important molecules in the RISK pathway，in heart of I/R damage. Thus we hypothesize that gastrin activates downstream RISK pathway to inhibit apoptosis and exert a protective effect against cardiac I/R injury. Thus，In this study, we use ischemia-reperfusion heart model and cell hypoxia-reoxygenation model to study the protective role of gastrin in the cardiac I/R injury and its underlying mechanism and explore new way to protect the heart of I/R damage .