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分子氢对心肌缺血再灌注损伤保护的机制研究-外科学(胸心外科)专业论文.docx

分子氢对心肌缺血再灌注损伤保护的机制研究-外科学(胸心外科)专业论文.docx

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分子氢对心肌缺血再灌注损伤保护的机制研究-外科学(胸心外科)专业论文

第二军医大学博士学位论文 第二军医大学博士学位论文 氢盐水 氢盐水对心肌缺血再灌注损伤保护的机制研究 - - PAGE 4 - - - PAGE 5 - Background Abstract With the development of society, the incidence of coronary artery disease is rising gradually. Of all the treatments for coronary artery disease, revascularization is the most important, which makes ischemia reperfusion (I/R) injury become the problem that almost every clinician has to deal with. Nowadays, I/R injury is viewed as a complex process involved with reactive oxygen species (ROS), intracellular calcium overload, neutrophil activation and change of permeability of cell membrane, and so on. Particularly ROS is considered to play an important role in I/R injury. However, there is few effective antioxidant drugs in the treatment of I/R injury. There are plenty of ROS produced in the inflammatory and ischemia process. Of these ROS, H2O2 and NO are considered to be signal molecule and have negligible toxic effect, while HO· and ONNO- are responsible for cell oxidative injury. In the past, clinicians found many powerful antioxidants to treat I/R injury, which were proved to be ineffective. It is because that powerful antioxidant will inevitably lead to endogenous redox imbalance. Hence, a selective antioxidant is necessary for the treatment of I/R injury. 2007, in 《nature medicine》Japanese scholar reported breath with 2% hydrogen could attenuate brain I/R injury by scavenging ROS selectively and effectively. Compared with previous antioxidant, hydrogen could selectively scavenge hydroxyl radical and peroxynitrite, which are most toxic in I/R injury. Then, there were other studies demonstrated that breath with hydrogen had a therapeutic effect on arteriosclerosis, liver and brain I/R injury. Objective This research is to study the possible cardio-protective effect of hydrogen rich saline on ischemia reperfusion injury in a rat model, and it also could provide theoretical basis for the use of hydrogen as a treatment for I/R injury clinically. Methods SD rats were ra

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