No abstract

Background and objective In recent years, coronary atherosclerotic heart disease become the major disease which is harmful to human health with a rising the trend of incidence. The world health organisation (WHO) predicts that by 2020 cardiovascular disease will become the primary cause of death in the world and Acute myocardial infarction as the most serious coronary heart disease type will become a culprit undoubtedly. Opening occlusion blood vessels early can effectively restore myocardial blood reperfusion, and can effectively save myocardial ischemic heart muscle, but ischemic reperfusion injury caused by reperfusion may lead to further myocardial cell death and cardiac function obstacle. Hyperbaric oxygen has been widely used in clinical, and played a good effect in the treatment of many diseases. The aim of this research is mainly to observe and discusses the infl uence and function mechanism of hyperbaric oxygen pretreatment on myocardial ischemia reperfusion (MIR) injury in rats. Methods Specifi c pathogen-free adult male Wistar rats weighing 200 to 250 g were used for the study provided by Laboratory animal center of Bethune medical college of Jilin University, and rats were divided into Control group, Irgroup, HBOpre+IR group randomly. Rats were exposed to 100% O 2 (hyperbaric oxygenation, HBO) for 60 min in a hyperbaric chamber daily. Rats exposed to hyperbaric conditions were allowed to recover for seven days before heart preparation. The rats received intraperitoneal injection of 20% Urethane, hearts were excised and immediately connected to an aortic cannula, and then perfused at a constant pressure in a non-circulating Langendorff mode with Krebs-Henseleit buffer solution, connect to BL-420 Biological function system. We record the data of HR, LVSP, ±dp/dtmax for different periods. After each experiment, we determined the activity of SOD and the quality of MDA, calculated myocardial infarction size with TTC dyeing, and observed the change of myocardial ultrastructure with HE dyeing. Last, we detected the expression of caspase-3, Bcl-2 and Bax in myocardial cells with immunohistochemical, and cardiomyocyte apoptosis with TUNEL.