CAJ | 학술논문

目的评价咪达唑仑和异丙酚对急性心肌梗死大鼠血清血管内皮生长因子(VEGF)浓度及粒细胞集落刺激因子(G-CSF)药物动员骨髓干细胞效果的影响.方法雄性Wistar大鼠36只,体重250 ～ 280 g,采用结扎左冠状动脉前降支的方法制备急性心肌梗死模型,采用腹腔连续注射G-CSF 5d进行药物动员,于药物动员后第7天,按照随机数字表法,将大鼠随机分为G-CSF组(G组)、咪达唑仑组(M组)及异丙酚组(P组),每组12只.G组以0.5 ml/h的速率股静脉输注生理盐水6h；M组股静脉输注咪达唑仑0.05 mg·kg-·h-1 6 h;P组股静脉输注异丙酚5mg·kg-1 ·h-16 h.于给药完毕后经股静脉取血,采用流式细胞仅测定CD34+单核细胞( CD34+ MNC)和内皮祖细胞(EPCs)数目,采用ELISA法测定血清VEGF浓度.于心肌梗死后4周每组随机取6只大鼠测定左心室舒张末压(LVEDP)、最大收缩速率(+dp/dtmax)和最大舒张速率(- dp/max).结果与G组比较,M组CD34+MNC及EPCs细胞数目增加,血清VEGF浓度升高,LVEDP下降,-dp/dtmax的绝对值升高(P＜0.05),P组LVEDP下降,- dp/dtmax的绝对值升高(P＜0.05)；与P组比较,M组CD34+MNC及EPCs细胞数目增加,血清VEGF浓度升高,LVEDP下降,- dp/dtmax的绝对值升高(P＜0.05).结论咪达唑仑可促进VEGF的释放,加强G-CSF动员骨髓干细胞的作用,改善急性心肌梗死后大鼠的心脏功能；异丙酚不能促进VEGF的释放及无骨髓干细胞动员的作用.
목적 평개미체서륜화이병분대급성심기경사대서혈청혈관내피생장인자(VEGF)농도급립세포집락자격인자(G-CSF)약물동원골수간세포효과적영향.방법 웅성Wistar대서36지,체중250 ～ 280 g,채용결찰좌관상동맥전강지적방법제비급성심기경사모형,채용복강련속주사G-CSF 5d진행약물동원,우약물동원후제7천,안조수궤수자표법,장대서수궤분위G-CSF조(G조)、미체서륜조(M조)급이병분조(P조),매조12지.G조이0.5 ml/h적속솔고정맥수주생리염수6h；M조고정맥수주미체서륜0.05 mg·kg-·h-1 6 h;P조고정맥수주이병분5mg·kg-1 ·h-16 h.우급약완필후경고정맥취혈,채용류식세포부측정CD34+단핵세포( CD34+ MNC)화내피조세포(EPCs)수목,채용ELISA법측정혈청VEGF농도.우심기경사후4주매조수궤취6지대서측정좌심실서장말압(LVEDP)、최대수축속솔(+dp/dtmax)화최대서장속솔(- dp/max).결과 여G조비교,M조CD34+MNC급EPCs세포수목증가,혈청VEGF농도승고,LVEDP하강,-dp/dtmax적절대치승고(P＜0.05),P조LVEDP하강,- dp/dtmax적절대치승고(P＜0.05)；여P조비교,M조CD34+MNC급EPCs세포수목증가,혈청VEGF농도승고,LVEDP하강,- dp/dtmax적절대치승고(P＜0.05).결론 미체서륜가촉진VEGF적석방,가강G-CSF동원골수간세포적작용,개선급성심기경사후대서적심장공능；이병분불능촉진VEGF적석방급무골수간세포동원적작용.
Objective To investigate the effect of propofol and midazolam on the serum vascular endothe lial growth factor (VEGF) concentration and granulocyte colony-stimulating factor (G-CSF)-induced bone marrow stem cell (BMSC) mobilization after acute myocardial infarction in rats.Methods Thirty-six male Wistar rats,weighing 250-280 g,were anesthetized with intraperitonel 1％ pentobarbital 45 mg/kg.Acute myocardial infarct was induced by ligation of left anterior descending branch of coronary artery.BMSC mobilization was induced by intraperitoneal injection of G-CSF for 5 days.On 7th day after BMSC mobilization,the rats were equally and randomly divided into three groups:G-CSF group (group G),midazolam group (group M) and propofol group (group P).In group G,normal saline was continuously infused via the femoral vein at a rate of 0.5 ml/h for 6 h.In group M,midazolam was infused via the femoral vein at 0.05 mg· kg - 1 · h- 1 for 6 h.In group P,propofol was infused via the femoral vein at 5 mg·kg1 -h-1 for 6 h.Blood samples were obtained from the femoral vein after administration to determine the number of CD34+ monocyte (CD34+ MNC) and endothelial progenitor cells (EPCs) by flow cytometry and the serum concentration of VEGF by ELISA.Six rats from each group were chosen 4 weeks after myocardial infarction for measurement of the left ventricular end-diastolic pressure (LVEDP) and ± dp/dtmax Results Compared with group G,the number of CD34 + MNC and EPCs,the serum concentration of VEGF,and the absolute value of - dp/dtmax were significantly increased,while LVEDP was significantly decreased in group ( P ＜0.05),and LVEDP was significantly decreased,and the absolute value of - dp/dtmax was significantly increased in group P ( P ＜ 0.05).Compared with group P,the number of CD34+ MNC and EPCs,the serum concentration of VEGF,and the absolute value of - dp/dtmax were significantly increased,while LVEDP was significantly decreased in group M (P ＜ 0.05).Conclusion Midazolam can promote the release of VEGF,strengthen G-CSF-induced BMSC mobilization and improve the cardiac function after acute myocardial infarction in rats.Propofol can not promote the release of VEGF and produce G-CSF-induced BMSC mobilization after acute myocardial infarction in rats.