| It had been demonstrated that bone marrow stem cells (BMCs)were mobilized to circulating blood after acute myocardial infarction.The BMCs stimulus was vascular endothelial growth factor(VEGF) and/or granulocyte colony-stimulating factor(G-CSF)and other cytokines.After the cells entered the circulating blood,adhesion molecules expressed at the injury site mediated attachment to endothelial cells.Finally tissue-directed differentiation within the injured organ was probably influenced both by cell-to-cell contact and by growth factors.Altough acute myocardial infarction could mobilize BMCs,the counts which BMCs could enter the circulating blood were limited.The study of medcine mobilizing BMCs were gradully increased. Chronic myocardial injury often become dilated cardiomyopathy,So,it was important to prevent left ventricular from dilating after infarction.So far, There were few reasearch on the relationship of mobilization of BMCs and prevention of dilated cardiomyopathy with medicine treatment. Scientists had applied cardiac toxic medicine to induce the animal model of dilated cardiomyopathy,but one defect which animal experiment need more time was exist. [Objective]:In this study, the new methods of animal model of dilated cardiomyopathy had been established. Which we examined whether CD34-positive cells (CD34+)were mobilized in rat with chronic myocardial injury. Whether compound danshen dripping pill(CDDP) and Fluvastatin could mobilize BMCs to prevent the dilation of cardiac cavity. [Methods]: SD rats were divided randomly into four groups:(1)group C(control)(;2)group I:treated with posterior 　pituitrin 　(20u/kg/w) and furanzolidone(0.2mg/kg/d).(3)group I+D and group I+S:interfered with CDDP(300mg/kg/d)or fluvastain(20mg/kg/d)every day. The posteriorpituitrin and furanzolidone treatment-induced dilated cardiomyopathy were established.The blood were acquired from rat orbital vein at the end of the week 1,3,6. Lympholyte seperation medium was used to seperate lympholyte The circulating CD34+ count was quantited in Flow cytometry.The LVESD,LVEDD,LVEF,LVEDP,±dp/dtmax were detected in Echocardiogram(UCG) at the end of the week 6. myocardial pathology were examined. [Results]:(1)The animal model of dilated cardiomyopathy had been establised successfully。At the end of 6 weeks, compared with group C, The HW/BW ratio in group I was higher than that in group C(3.59±0.22 vs 3.09±0.09,k/kg.p<0.01),the LVESD and LVEDD in group I were significantly higher (2.51±0.35 vs 1.48±0.18;6.72±0.29 vs 5.77±0.43,mm.p<0.01) , but LVEF was lower (94.03 ±2.49 vs 98.28 ±0.51,p<0.05),Meanwhile,the ±dp/dtmax in group I were lower obviously (587.33±89.10 vs 715.46±83.16,p<0.01;456.23±59.19.vs.596.97±53.34,kpa/s.p<0.01). The fibrosis tissue of myocardium was obvious in group I compared with group C (2) The HW/BW ratio in group I+D or group I+S was lower than that in group I(2.83±0.13, 3.07±0.19 vs 3.59±0.22 g/kg,p<0.05).Compared group I, the LVESD and LVEDD in group I+D or group I+S were significantly lower (1.81 ±0.16 vs 2.51 ±0.35;6.03 ±0.39 vs 6.72 ±0.29,mm.p<0.05);(1.80 ±0.28 vs 2.51 ±0.35;5.72 ±0.80 vs 6.72 ±0.29,mm.p<0.05). but LVEF was higher(97.06±1.03,96.76±0.86 vs94.03±2.49,p<0.05). Meanwhile,the ±dp/dtmax in group I+D or group I+S were higher compared with those in group B(661.82±71.04,714.55±105.42 vs 587.33 ±89.10,kpa/s.p<0.05). The fibrosis tissue of myocardium was not obvious in group I+D or group I+S. (3)Compared with group C,the ratio of CD34+ of group I was higher at the end of the week 1 (1.61±0.54 vs 0.29±0.20,p<0.01),The ratio of CD34+ of group I+D and I+S was higher than that in group I at the end of the week 3 or 6(3.84±2.10,3.02±1.22 vs 1.61±0.54,p<0.01;1.08±1.46,1.27±1.13 vs 0.62±0.53,p>0.05;1.27±1.13,1.06±1.17 vs 0.41±0.32,p>0.05). But no statistical difference. [Conclusion]: (1)The animal model of dilated cardiomyopathy could be established by posterior pituitrin and furanzolidone quickly. (2)BMCs could be mobilized during the early chronic myocardium injury phase. (3) The degree of left ventricular dilation alleviated obviously with CDDP and Fluvastatin intervene. (4)Fluvastain and CDDP could mobilize BMCs, which might be relate to prevent or alleviate cardiac injury.
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