中文摘要：

目的探讨粒细胞集落刺激因子（G-CSF）对慢性心肌缺血的保护作用及其机制。方法雄性日本大耳白兔为研究对象,开胸后不全结扎冠状动脉左前降支,建立慢性心肌缺血模型。将成功制备的模型兔随机分为2组,即G-CSF干预组和对照组。应用流式细胞术测定外周血CD34＋细胞百分率,应用免疫组化法测定心肌组织CD34＋细胞归巢和vWF的表达。结果 G-CSF明显提高慢性心肌缺血模型兔的生存率,增加外周血CD34＋细胞百分率,促进缺血心肌组织中CD34＋细胞归巢和vWF表达。结论 G-CSF对兔慢性心肌缺血损伤具有明显保护作用,其机制与外周血CD34＋细胞动员和归巢于缺血心肌以及促进血管新生有关。

英文摘要：

Objective To investigate the protective effects and mechanisms of granulocyte-colony-stimulating factor （G-CSF） on a rabbit model of chronic myocardial ischemia. Methods Myocardial ischemia models were created by partial ligation of the left anterior descending coronary artery in Japanese white male rabbits. Rabbits were subcutaneously injected with G-CSF （G-CSF group） or saline （control group） for 6 days after myocardial ischemia. The percentage of CD34-positive cells in the peripheral blood was evaluated by flow cytometry, and CD34-positive cells homing and vWF expression in the ischemic myocardium were determined by immunohistochemistry. Results Rabbits in G-CSF group had a higher survival rate than those in control group （P〈0. 05）. Immunohistochemistry of the ischemie myocardium showed that compared with control group, G-CSF group had increased homing of CD34-positive cells on day 7 post-surgery, and more vessels on day 28 post-surgery by anti-von Willebrand factor staining. In addition, we observed an increase in the percentage of CD34-positive cells in the peripheral blood in G-CSF group. Conclusion G-CSF produces an obvious protective effect against chronic myocardial ischemia in rabbits by increasing stem cell mobilization, homing to ischemic myocardium and accelerating neovascularization.