本文關(guān)鍵詞： 生理性缺血訓練 心肌缺血 側(cè)支循環(huán) 內(nèi)皮祖細胞 血管內(nèi)皮生長因子　出處：《南京醫(yī)科大學》2014年碩士論文　論文類型：學位論文

【摘要】：目的：探討EPCs動員在生理性缺血訓練促進遠隔缺血心肌側(cè)支循環(huán)生成過程中的作用。 方法：42只兔進行可控性心肌缺血造模,造模成功后隨機分入以下6組：①假手術(shù)組(Sham-operated group, SO);②單純生理性缺血訓練組(Training only group,TO)；③單純心肌缺血組(Myocardial ischemia group, MI);④生理性缺血訓練組(Physiological ischemic training group, PIT);⑤阿托伐他汀組(EPC promotor group, PIT+);⑥雷帕霉素組(EPC inhibitor group, PIT-).生理性缺血訓練共4周,每次3分鐘,間隔5分鐘,每周訓練5天,每天訓練3次；心肌缺血刺激共4周,每次2分鐘,間隔10分鐘,每周刺激5天,每天刺激2次。實驗終點時,處死動物取材,進行實驗室檢測：ELISA法檢測外周血中VEGF含量；Western blot法檢測缺血心肌中VEGF表達；流式細胞術(shù)檢測外周血和缺血心肌中EPCs數(shù)量；微球技術(shù)檢測缺血心肌側(cè)支循環(huán)血流量�？紤]到各組VEGF蛋白含量、EPCs數(shù)量和冠狀動脈側(cè)支循環(huán)血流量的改變量的實驗數(shù)據(jù)并不符合正態(tài)分布,因此本研究采用非線性分析方法來計算各組間的差異,同時使用盒須圖來呈現(xiàn)統(tǒng)計結(jié)果。 結(jié)果：4周PIT后,VEGF含量在PIT組和PIT+組顯著增加,與SO組、TO組和MI組相比,外周血和缺血心肌中VEGF含量在PIT組顯著增加,結(jié)果具有統(tǒng)計學意義。PIT+組的EPCs數(shù)量在外周血和缺血心肌中均顯著高于其他各組,PIT組與其他各組相比,外周血EPCs數(shù)量的差異同樣具有統(tǒng)計學意義。CCBF和CCBF/CBF在PIT+組和PIT組顯著高于SO組、TO組和MI組。PIT-組的各項指標與SO組和TO組相比,差異均無統(tǒng)計學意義。EPCs數(shù)量的增加最高有43%可以被VEGF含量的增加解釋,CCBF和CCBF/CBF的增加最高有90%可以被EPCs數(shù)量的增加解釋。 結(jié)論：PIT可促進EPCs動員,通過其遠隔效應(yīng)歸巢到缺血心肌生成側(cè)支循環(huán),改善冠脈血流,最終實現(xiàn)“生物搭橋”；通過促進和抑制EPCs,證實EPCs在PIT介導的缺血心肌側(cè)支循環(huán)生成過程中具有重要作用。
[Abstract]:Aim: to investigate the role of EPCs mobilization in physiological ischemic training to promote collateral circulation formation in distant ischemic myocardium. Methods Twenty two rabbits were induced by controlled myocardial ischemia and were randomly divided into the following 6 groups: the sham-operated group (SOP) and the sham-operated group (SOP). (2) training only group in physiologic ischemic training group; 3Myocardial ischemia group; 4Physiological ischemic training group; 5EPC promotor group, PIT group in Atto vastatin group; 6in rapamycin group, EPC inhibitor group, PIT-0.Physiologic ischemia training lasted for 4 weeks, 3 minutes each time, the interval was 5 minutes, 5 days per week. Training 3 times a day; Myocardial ischemia was stimulated for 4 weeks, 2 minutes each time, 10 minutes interval, 5 days a week, 2 times a day. At the end of the experiment, the animals were sacrificed. The content of VEGF in peripheral blood was detected by the method of Elisa. The expression of VEGF in ischemic myocardium was detected by Western blot method. The number of EPCs in peripheral blood and ischemic myocardium was detected by flow cytometry. Microsphere technique was used to measure the collateral circulation blood flow in ischemic myocardium. The experimental data of the number of VEGF and the changes of coronary collateral circulation blood flow were not in accordance with normal distribution considering the content of VEGF protein in each group. Therefore, the nonlinear analysis method is used to calculate the differences among groups, and the box chart is used to present the statistical results. Results after 4 weeks of PIT, the content of VEGF in PIT group and PIT group was significantly higher than that in so group and MI group. The content of VEGF in peripheral blood and ischemic myocardium was significantly increased in PIT group. The results showed that the number of EPCs in Pit group was significantly higher than that in other groups in peripheral blood and ischemic myocardium. Compared with other groups, the number of EPCs in peripheral blood of PIT group was significantly higher than that of so group. CCBF and CCBF/CBF in PIT group and PIT group were significantly higher than that in so group. Compared with so group and to group, the increase of the number of VEGF in to group and MI group could be explained by the increase of VEGF content. Up to 90% of the increase in CCBF and CCBF/CBF can be explained by the increase in the number of EPCs. Conclusion EPCs mobilization can be promoted by the effect of wet-pit, which can homing to collateral circulation of ischemic myocardium, improve coronary blood flow, and finally realize "biological bypass graft". By promoting and inhibiting EPCs, it is confirmed that EPCs plays an important role in the formation of collateral circulation in ischemic myocardium mediated by PIT.
【學位授予單位】：南京醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2014
【分類號】：R87

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