| Background and objective: It is generally believed that mature body's myocardial cell lacks the ability to differentiate and cannot be regenerated. Once the myocardial cells are damaged, there will be hyaline degeneration and fibroatrophy and the damaged cells can only be repaired via scar repairing. At present, the therapies for injury of myocardial cell include drug, intervention and operation but only for resumption of perfusion rather than repairing or reversing the necrotic myocardium. The key point to prevent heart failure and lower mortality is to promote myocardial cell regeneration in the infarct zones, to increase the number of myocardial cells, to prevent ventricular remodeling. It is found that bone marrow stem cells can migrate automatically to the damaged myocardial areas and differentiate to myocytes and vascular endothelial cells regenerating infracted myocardium. However, in general, bone marrow stem cells coming to peripheral blood circulation and migrating to infarcted zones are extremely rare, and the repairing function is very limited. So use mobilizing agents to "drive" bone marrow stem cells to peripheral blood for increase of stem cells in peripheral blood, which maystimulate stem cells to migrate to infracted area and further differentiate for the increase of functional myocytes and formation of new born vessels, improving the repairing of myocardial tissues. Granulocyte colony stimulating factor(G-CSF) is a powerful mobilizing agent of bone marrow stem cells. Administration of G-CSF can mobilizes stem cells from bone marrow to peripheral blood. The number of circulating stem cells can be increased scores of times of that before mobilization. In the present study, after using G-CSF to mobilize autologous bone marrow stem cells in myocardial infarction rats, we observed the stem cells' translocation to the infarcted zones, proliferation and differentiation, the influence of myocardial basic structure, infarct size, neovascularization and heart function. And we investigated the possible mechanism at last. Methods: 260 male and healthy Wistar rats(10~12 months old) were injected subcutaneously with 170mg/kg of ISO one-time to duplicate the model of acute myocardial infarction(AMI). After injection of ISO, they were divided into 5 groups at random: ISO+G-CSF mobilized group(n=60), ISO+NS group(n=60), normal+G-CSF mobilized group(n=60), acute myocardial infarction group(n=60) and normal control group(n=20). The levels of serum CK-MB and LDH-1 were tested before and after the duplicatation of AMI model. After the duplicatation for 24rK 48h and 2w, the blood flow dynamic index and coefficient of heart function of each rat were detected. Hearts wereharvested from 24h to 2w after administration of ISO for histopathological examination. Immunohistochemistry and HE stain were used to detect infiltration of CD34 monocytes and the regeneration of myocytes and angiogenesis in the infarct zones. The degree of myocardial damage in pathology was observed. The biofunction laboratory system(BL-420E system) was applied to measure the infarct sizes. A section of the whole heart long axial surface with 3um thick was cut every other l00um, 4 in all with HE stain, via which the morphological characteristics and arranging pattern of cells were observed. The expression of CD34> BrdU positive cells-, VIII factor^ VEGF and flk-1 in the part of ischemia were detected by immunohistochemistry SABC method according to the instructions of reagent box. At last, the mortality of rats was calculated.Results: (1) 24h after the duplicatation of rat MI model, the level of serum of CK-MB and LDH-1 increased in ISO+G-CSF mobilized group> ISO+NS group and acute myocardial infarction group compared with normal control group(all P< 0.05).The level of serum of CK-MB and LDH-1 decreased in ISO+G-CSF mobilized group compared with ISO+NS group and acute myocardial infarction group(although PXX05). (2) SBP DBP LVSP and LV 眃p/dtmaxin ISO+G-CSF mobilized group were higher than those of ISO+...
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