| Part oneMobilized Stem Cells by G-CSF repair the infarcted heart and improvefunctionObjective: This study was designed to observe the role of G-CSF in repairing infarct area and improving function in rats with myocardial infarction. Methods: Twenty-nine rats were randomized to there groups: GAMI (n=9), AMI (n=10) and SO (n=10). The coronary artery was ligated in GAMI and AMI groups, and sham-operation was performed in SO group. Rats of GAMI group were injected with G-CSF(50μg/kg/day) for seven days. Saline was given by the same manner in sham-operated rats and AMI groups. After four weeks of infarction, hemodynamic parameters were measured with catheterization, and the size of infarct area and the density ot little vessels in infract and peri-infarct area were measured under a microscope. Results: Three rats in AMI group died on the third, seventh and eighth day after myocardial infarction. No rats died in GAMI and AMI groups. Compared with that of SO group, LVSP (p<0.01), dp/dtmax (p< 0.01) and dp/dtmin (p<0.05) of AMI were decreased, but LEVDP (p<0. 01) was increased. And in GAMI group, dp/dtmax (p < 0.05) was also decreased, LEVDP (p<0.01) was increased . However, LVSP (p<0.05) and dp/dtmin (p < 0.05) were no statistic significant in GAMI group. Compared with that of AMI group, LVSP, dp/dtmax and dp/dtmin were increased, LEVDP was decreased in GAMI group(p < 0.01, p < 0.01, p <0.05, p < 0.05 respectively). We also found that the size of infarct regions was reduced and the density ot little vessels was enhanced in GAMI group(p<0.01, p < 0.05 respectively, versus AMI group). Conclusion: The treatment of G-CSF can reduce the size of infarct zone , enhance the number of little vessels and improve the function in rats with myocardial infarction.Part twoEffects of G-CSF on T lymphocyte subpopulations of myocardium in ratswith acute myocardial infarctionObjective: The aim of this study was to investigate T lymphocyte subsets changes by treatment of G-CSF in acute myocardial infarction rats. Methods: Twenty-nine rats were randomized to there groups: GAMI (n=9), AMI (n=10) and S0(n=10). The coronary artery was ligated in GAMI and AMI groups, and sham-operation was performed in SO group. Rats of GAMI group were injected with G-CSF(50 y g/kg/day) for seven days. Saline was given by the same manner in sham-operated rats and AMI groups. After four weeks of infarction, the number of CD3+, CD4+ and CD8+cells per field of a microscope and CD4+/CD8+ ratio was obtained through the stain of immunohistochemistry. Results: Three rats in AMI group died on the third, seventh and eighth day after myocardial infarction. No rats died in GAMI and AMI groups. A significant decrease in the number of CD3+ and CD8+ cells per field combined with a significant increase in CD4VCD8* ratio were documented in GAMI group (p < 0. 01, p < 0. 01, p < 0.01 respectively, versus AMI group) . There were no statistic significant in that of CD4+ cells between AMI and SO groups. Conclusion: The treatment of G-CSF can reduce the number of CD3+, and CD8+ per field , enhance CD4+/CD8+ ratio in rats with myocardial infarction. These findings suggests G-CSF may play a important role in improving immune response induced by T lymphocyte in acute myocardial infarction rats.Part threeInfluence of G-CSF on cardiomyocyte apotosis in rats with acutemyocardial infarctionObjective: This study was undertaken to evaluate the effect of G-CSF on cardiomyocyte apotosis in rats with myocardial infarction and to correlate this change with left ventricular function. Methods: Twenty-nine rats were randomized to there groups: GAMI(n=9),"AMI(n=10) and S0(n=10). The coronary artery was ligated in GAMI and AMI groups, and sham-operation was performed in SO group. Rats of GAMI group were injected with G-CSF(50 u g/kg/day) for seven days. Saline was given by the same manner in sham-operated rats and AMI groups. After four weeks ofinfarction, heraodynamic parameters were measured with catheterization, and the cardiomyocyte apotosis was examined by in suit TDT-mediated dUTP nick. Results: Three rats in AMI group died on the third, seventh and eighth day after myocardial infarction. No rats died in GAMI and AMI groups. In comparison with SO group, cardiomyocyte apopotic index(APOI) of AMI group was increased significantly (p<0. 05), but the difference of that between GAMI group was no significant.We also found a decreasing of APOI in GAMI group compared with AMI group in the peri-infarct zone , remote zone or overall( p < 0.01, p < 0. 05, p < 0. 01 respectively). Moreover, LVEDP presented positive relation with APOI of the peri-infarct zone(r=0. 872, p<0. 01). Conclusion: The results of this study indicated G-CSF can inhibit cardiomyocyte apoptosis in acute myocardial infarction rats and improve left ventricular function by that.Part fourCD34+ cells mobilized by G-CSF home to the heart and express GATA-4 inrats with myocardial infarctionObjective: This part sought to confirm CD34+ cells mobilized by G-CSF can home to the heart and express GATA-4 in rats with myocardial infarction. Methods: Twenty-eight rats were randomized to there groups: GAMI (n=9), AMI (n=9) and S0(n=10). The coronary artery was ligated in GAMI and AMI groups, and sham-operation was performed in SO group. Rats of GAMI group were injected with G-CSF(50 u g/kg/day) for four days. Saline was given by the same manner in sham-operated rats and AMI groups. After five days of myocardial infarction, CD34+ cells expressing GATA-4 were tested through immunofluorescin histochemistry technique. Results: One rat in AMI group died on second day after myocardial infarction. No rats died in GAMI and AMI groups. Positive rate of CD34+ cells expressing GATA-4 was 44.4%, and 95% confidence interval(CI) was (14%, 79%) in GAMI group. That show a statistic significant.That rate of AMI group was 12.5%, and 95% CI was (0,37%). In SO group, the positive rate was 0, and 95% CI was (0,31%). There were no statistic significant in AMI and SO groups. Conclusion: CD34+ cells expressing GATA-4 can exist in myocardium in acute myocardial infarction rats. This phenomenon hint that CD34+ cells mobilized by G-CSF can home to the heart and transdifferentiate into cardiomyocyte lineage.
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