自体骨髓源干细胞动员对大鼠急性心肌梗死治疗作用的实验研究

目的初步探讨自体骨髓源干细胞动员对大鼠急性心肌梗死的治疗作用及其机制。方法采用粒细胞集落刺激因子（G-CSF）皮下注射动员自体骨髓源干细胞,观察其对心肌梗死动物模型的影响。选择SD大鼠90只,开胸结扎左冠状动脉前降支制作急性心肌梗死模型,随机分为3组:A组为双时相G-CSF动员组:第一时相于模型制备3 h后皮下注射生理盐水稀释的G-CSF40μg·kg^-1/d,连续注射5 d（第0-4 d）,第二时相于第7 d开始,再连续注射5 d（第7-11 d）;B组为单时相G-CSF动员组:仅于模型制备3 h后连续5 d皮下注射G-CSF、,剂量同A组;C组为对照组:于模型制备3 h后连续5 d皮下注射等量生理盐水。对各组大鼠采用累积法5-溴-2-脱氧尿苷（BrdU）腹腔注射,剂量为50 mg·kg^-1/d,术前2 d开始连用7 d。3组大鼠分别于不同时间点采血,流式细胞术检测外周血CD34+/WBC的变化趋势、酶联免疫法（ELISA）检测血清血管内皮生长因子（VEGF）变化;不同时间点心脏超声检测心功能后取心脏,三苯基氯化四氮唑（TTC）染色法测定心肌梗死面积,苏木精-伊红（HE）染色法观察心肌组织病理变化,免疫组织化学法检测梗死区域CD34+细胞、BrdU阳性细胞、Ⅷ因子的表达,原位末端标记法（TUNEL）原位标记检测细胞的凋亡。结果双时相G-CSF骨髓源干细胞动员组心肌梗死大鼠外周血CD34+/WBC比例明显升高,最高为0.508%±0.030%,持续1周左右维持在正常值4～7倍的水平;血清中VEGF表达水平提高,最高为20.23±0.51 pg/ml,同其它各组比较,差异有统计学意义（P<0.05）。28 d后双时相动员组心肌梗死大鼠左室射血分数为68.96%±5.79%,较单时相组52.80%±3.21%和对照组40.22%±3.79%均明显改善,心肌梗死面积小,病理损伤程度轻,凋亡细胞减少,梗死区及周边区心肌中可见有CD34+细胞、BrdU阳性细胞的高表达和较高的新生血管密度,差异有统计学?     

经冠状动脉注射骨髓单个核细胞治疗缺血性心肌损伤的实验研究

目的　证实骨髓干细胞心肌内移植治疗对心脏功能的改善和促血管新生作用。方法　小型猪冠状动脉结扎制备心肌梗死模型 ,然后经冠状动脉内注射骨髓单个核细胞 ,术后 3周用超声心动图以及左心室造影检测心功能的变化 ,核素心肌显像观察心肌灌注的情况 ,冠状动脉造影观察侧支循环的形成 ,免疫组化计数血管密度。结果　心肌梗死小型猪冠状动脉注射骨髓单个核细胞后 ,左心室造影显示左室 dP dtmax与对照组比较增高。核素心肌显像显示冠状动脉注射骨髓单个核细胞后心肌灌注显著改善。移植治疗后冠状动脉造影显示有侧支循环形成 ,血管密度计数比对照组增加了5 2 2 % (5 6 6± 11 7 mm2 vs 37 2± 8 4 mm2 ,P <0 0 5 )。结论　骨髓单个核细胞心肌内移植可能通过促进血管新生改善心脏收缩功能。     

碱性成纤维细胞生长因子基因对猪缺血心肌侧支血管生成的作用

目的探讨经导管冠状动脉内注射碱性成纤维细胞生长因子(bFGF)基因(pcDNA3-bFGF)对猪缺血心肌侧支血管生成的作用。方法实验猪分为3组:手术对照组(n=6)、bFGF基因左冠状动脉注射组(n=6)和bFGF基因右冠状动脉注射组(n=6)。开胸结扎冠状动脉左回旋支(LCX),建立急性心肌梗死动物模型。术后2周,分别行选择性冠状动脉造影,并经导管冠状动脉内注射pcD-NA3-bFGF 2 000μg。给药后2周,再次行选择性冠状动脉造影观察冠状动脉侧支血管形成情况,并通过病理切片光镜观察、免疫组化染色进行血管计数,观察猪缺血心肌侧支血管生成情况。结果(1)病理切片及免疫组化染色结果显示左、右冠状动脉注射基因组血管计数较对照组明显增加;(2)术后4周选择性冠状动脉造影显示左、右冠状动脉注射基因组侧支血管明显多于对照组,左冠状动脉注射基因组侧支血管多于右冠状动脉基因注射组。结论经导管冠状动脉内注射bFGF基因能促进猪缺血心肌侧支血管生成。     

动员自体骨髓干细胞对急性心肌梗死大鼠心功能的影响

目的:探讨联合应用粒细胞集落刺激因子（G-CSF）和干细胞因子（SCF）动员心肌梗死大鼠的骨髓干细胞并观察对心功能的影响及探讨其可能机制。方法:雄性W istar大鼠40只经结扎冠状动脉前降支制作心肌梗死模型后随机分为两组。①动员组:皮下注射rh-CSF和rh-SCF。②对照组:皮下注射等量生理盐水。28 d后通过测定血流动力学观察大鼠心功能变化,通过伊文氏蓝-TTC染色方法观察心肌梗死范围的变化。通过HE染色方法、免疫荧光标记染色和双重免疫荧光标记染色观察心肌梗死范围内心肌纤维化、血管和心肌再生的变化。结果:动员组心肌组织梗死范围内成纤维细胞增生程度轻,新生血管和心肌细胞的特异蛋白染色阳性,与对照组比较,动员组左室收缩压显著增大（P<0.05）,舒张末压显著减小（P<0.05）,左室压上升/下降变化最大速率显著增快（P<0.05）。动员组的缺血范围和心肌梗死的范围比对照组均有所缩小（P<0.05）。结论:G-CSF和SCF动员骨髓干细胞可以改善心肌梗死后大鼠的心功能。     

重组腺相关病毒介导CD151转染心肌梗死小型猪促进心肌功能性血管形成

目的 观察重组腺相关病毒(rAAV)介导的CD151基因转染促小型猪心肌梗死后心肌血管形成的有效性.方法 结扎小型猪冠状动脉左前降支建立心肌梗死模型,梗死区及梗死周围心肌分别注射rAAV-CD151、rAAV-anti-CD151和rAAV-绿色荧光蛋白(rAAV-GVP).8周后用Western blot分析心肌组织CD151蛋白表达,免疫组化检测心肌微血管密度和小动脉密度,用13N-NH3电子发射计算机断层心脏显影(PET)评价心肌血流灌注.结果 CD151基因转染促进心肌组织局部CD151高表达.rAAV-CD151组心肌微血管密度为(83.8±6.7)个/mm2,明显高于正常对照组的(33.2±4.5)个/mm2和rAAV-GFP组的(41.6±5.6)个/mm2,均P＜0.05;rAAV-CD151组小动脉密度为(16.4±2.5)个/mm2,也明显高于正常对照组的(6.6±2.3)个/mm2和rAAV-GFP组(8.4±1.6)个/mm2,均P＜0.05.rAAV-anti-CD151组心肌微血管密度和小动脉密度明显低于其他各组.13N-NH3 PET心肌血流灌注显像示rAAV-CD151组缺血区心肌血流灌注明显增加,rAAV-anti-CD151组血流灌注减少.结论 CD151基因转染能增加小型猪局部心肌组织的CD151表达,明显增加缺血心肌微血管和小动脉的生成,并显著增加心肌血流灌注.     

碱性成纤维细胞生长因子基因对猪缺血心肌心功能的影响

目的探讨经导管冠状动脉内注射碱性成纤维细胞生长因子基因(pcDNA3-bFGF),对猪缺血心肌心功能的影响。方法构建真核表达质粒pcDNA3-bFGF。开胸结扎猪冠状动脉左回旋支(LCX),建立急性心肌梗死动物模型。实验动物分为三组:手术对照组(n=6),bFGF基因左冠状动脉注射组(n=6),bFGF基因右冠状动脉注射组(n=6)。术后2周,分别行选择性冠状动脉造影,并经导管冠状动脉内注射pcDNA3-bFGF2000μg。术后4周,通过超声心动图测定左心室射血分数(LVEF),评估左心室收缩功能,并再次行选择性冠状动脉造影,观察冠状动脉侧枝血管新生情况,并通过压力监测装置观察不同组动物左心室舒张末压(LVEDP)。结果(1)术后4周超声心动图示左、右冠状动脉注射基因组LVEF值高于手术对照组,LVDEP低于手术对照组;(2)选择性冠状动脉造影显示,术后4周左右冠状动脉注射基因组侧枝血管明显多于对照组,左冠状动脉注射基因组,侧枝血管多于右冠状动脉基因注射组。结论经导管冠状动脉内注射bFGF基因,能促进猪缺血心肌血管新生,改善缺血心肌血供,改善心功能。     

自体骨髓干细胞移植治疗慢性缺血性心脏病患者的有效性

目的 对自体骨髓干细胞(bone marrow-derived cells,BMC)移植治疗慢性缺血性心脏病的有效性进行荟萃分析.方法 全面检索MEDLINE、EMBASE、Cochrane等数据库,人选研究满足以下条件:体现随机对照原则;以慢性缺血性心脏病患者为研究对象;移植细胞为非动员的自体BMC;BMC移植方式为经冠状动脉移植或直接心肌内注射.提取有关左心室射血分数、左心室舒张末期容积/腔径、左心室收缩末期容积/腔径及患者死亡的信息.应用RevMan 5.0软件及随机效应模型进行数据统计,应用STATA 10.0软件进行Meta回归分析评价异质性的来源;此外,亚组分析比较直接心肌内注射和经冠状动脉注射2种移植方式对移植效果的影响.结果 11项随机对照研究共纳入490例,其中移植组268例,对照组222例,平均随访6.6个月,移植组接受经冠状动脉或直接心肌内注射BMC,对照组接受生理盐水注射、自体血浆注射或不接受任何处理.与对照组相比,BMC移植组左室射血分数较对照组高4.63%(95%C/:2.42～6.84,P<0.01),而左心室舒张末期容积/腔径(标化均差-0.55,95%CI:-0.94～-0.17;P=0.005)和左心室收缩末期容积/腔径(标化均差-0.45,95%CI:-0.73～-0.17;P=0.002)均低于对照组.此外,移植组患者死亡也低于对照组(OR=0.42,95%CI:0.18～1.01,P=0.05).亚组分析显示直接心肌内注射较经冠状动脉移植更好地改善患者LVEF,Meta回归分析提示基线LVEF值越低的患者从自体BMC移植中获得的益处越大.结论 BMC移植治疗可显著改善慢性缺血性心脏病患者的LVEF,有效预防左心室舒张、收缩末期容积/腔径的扩大.     

血栓抽吸后联合药物注入在急性ST段抬高型心肌梗死患者急诊冠状动脉介入治疗中的应用

目的研究急诊冠状动脉介入治疗中血栓抽吸后联合替罗非班及维拉帕米冠状动脉内注射对急性ST段抬高型心肌梗死患者心肌灌注及预后的影响。方法纳入281例急性ST段抬高型心肌梗死拟行急诊PCI治疗患者,分为联合药物治疗组(即在常规对闭塞血管行血栓抽吸后即刻通过抽吸导管于闭塞处以远注入替罗非班及维拉帕米药物,其后再行球囊扩张或支架术)及对照组(对闭塞血管行血栓抽吸及球囊扩张后置入支架),术后进行为期6个月的随访,比较两组术后即刻冠状动脉血流及心肌灌注情况,半年内主要心脏不良事件(MACE)发生率及随访半年内左心室收缩功能。结果两组间入选时基本临床资料比较差异无显著性;两组间术后TIMI3级血流患者比例无明显差异(91.5%比89.3%,P=0.531);联合药物治疗组较对照组有更低的校正的TIMI血流帧数计数(CTFC)(21±6比25±8,P0.001),心肌灌注分级(TMPG)2~3级比例高于对照组(65.2%比52.1%,P0.001)。联合药物治疗组术后2 h心电图ST段回落50%患者比例高于对照组(66.7%比53.6%,P=0.025);两组患者术后半年内MACE发生率无明显差异(2.1%比3.6%,P=0.712)。联合药物治疗组半年后左心室射血分数(LVEF)值较对照组升高(50%±8%比46%±9%,P0.001),左心室舒张期末内径(LVEDd)值较对照组减小(47.6%±8.3%比52.6%±7.7%,P0.001)。结论急诊冠状动脉介入治疗术中血栓抽吸后于冠状动脉内注射替罗非班及维拉帕米能改善急性心肌梗死患者心肌水平的灌注,提高了左心室收缩功能,可能对改善患者的长期预后有一定的帮助。     

CD105抗体支架内再狭窄及血栓形成的实验研究

目的 探讨CD105抗体支架预防再狭窄及血栓形成的作用.方法 将CD105抗体支架(CD105支架组)、Cypher支架(Cypher支架组)及316L不锈钢金属裸支架(裸支架组)各30枚分别置入30只小型猪的冠状动脉内.术后7和14 d,通过冠状动脉造影对冠状动脉进行量化分析,以扫描电镜观察血管内皮的变化,并在光镜下观察血管形态学的改变.结果 术后7 d,CD105支架组、裸支架组支架内皮化积分均高于Cypher支架组(1.71 4±0.49、1.50 4±0.67比1.08±0.29,P均<0.05);CD105支架组[(23.8±3)%、(0.14±0.10)mm]、Cypher支架组[(21.7±2)%、(0.11±0.08)mm]管腔狭窄率和晚期管腔丢失与裸支架组[(24±3)%、(0.12±0.09)mm]差异无统计学意义.术后14 d,CD105支架组、Cypher支架组晚期管腔丢失小于裸支架组[(0.29±0.28)mm、(0.28±0.02)mln比(0.41±0.01)mm,P均<0.05];支架内皮化积分CD105支架组、裸支架组均高于Cypher支架组(1.78±0.49、1.50±0.67比1.08±0.29,P均<0.05),CD105支架组高于裸支架组(P<0.05);CD105支架组、Cypher支架组管腔狭窄率均小于裸支架组[(23.8±4)%、(24.2±2)%比(38.0±3)%,P均<0.05],CD105支架组与Cypher支架组差异无统计学意义.新生内膜面积CD105支架组、Cypher支架组小于裸支架组[(0.88±0.08)mm2、(0.89±0.12)mm2比(1.00±0.14)mm2,P均<0.05],CD105支架组与Cypher支架组差异无统计学意义.术后7和14 d,各组间损伤积分及炎症积分差异无统计学意义,且均无支架内血栓形成.术后7和14 d,扫描电镜显示CD105支架组血管内皮覆盖程度均明显高于Cypher支架组和裸支架组.结论 CD105抗体支架能有效预防支架内再狭窄及血栓形成.     

粒细胞集落刺激因子对大鼠肺动脉高压模型的影响

目的:探讨粒细胞集落刺激因子(G-CSF)对野百合碱(MCT)诱导的大鼠肺动脉高压(PAH)的治疗作用。方法:动物随机分为3组:正常对照组(CON组)、MCT组和MCT/G-CSF组,腹腔注射MCT诱导大鼠PAH模型,采用G-CSF腹腔注射动员自体骨髓干细胞(BMSC),动员结束后行肺组织CD34免疫组化染色,第5周分别对3组大鼠进行血流动力学检测,处死大鼠,取肺、右心组织行苏木素-伊红(HE)染色。结果:1.动员结束后第2天,CD34+细胞浸润至肺血管平滑肌层和血管内皮细胞周围,以及肺泡间隔内;2.实验第35天,MCT组大鼠肺小动脉管壁增厚、管腔明显狭窄,血流动力学指标明显高于CON组(P<0.01);3.MCT/G-CSF组肺血管病变明显改善、肺泡结构完整,血流动力学指标明显低于MCT组(P<0.05)。结论:G-CSF可以动员骨髓干细胞并归巢致受损肺组织内,部分逆转PAH的血流动力学和病理学改变、减缓PAH的进展,用于PAH的研究和治疗。     

Cardioprotective effects of granulocyte colony-stimulating factor in swine with chronic myocardial ischemia.

OBJECTIVES: The aim of this study was to investigate the effect of granulocyte colony-stimulating factor (G-CSF) on chronic myocardial ischemia in swine. BACKGROUND: We recently have reported that G-CSF prevents cardiac remodeling and dysfunction after acute myocardial infarction in mice and swine. It remains unclear whether G-CSF has beneficial effects on chronic myocardial ischemia. METHODS: An ameroid constrictor was placed on left circumflex coronary artery of swine. The presence of myocardial ischemia was verified at four weeks after the operation, and the animals were randomly assigned into the following two groups: 1) administration of vehicle (control group, n = 10), and 2) administration of G-CSF (10 microg/kg/day) for seven days (G-CSF group, n = 10). RESULTS: Echocardiographic examination revealed that the G-CSF treatment prevented left ventricular dilation and dysfunction at eight weeks after the operation. Stress echocardiography revealed that G-CSF ameliorated the regional contractility of chronic myocardial ischemia. Morphological analysis revealed that the extent of myocardial fibrosis of the ischemic region was less in the G-CSF group than in control group. There were more vessels and less apoptotic cells at the ischemic region of the heart of the G-CSF group than control group. Moreover, Akt1 was more strongly activated in the heart of the G-CSF group than control group. CONCLUSIONS: These findings suggest that G-CSF improves cardiac function of chronic myocardial ischemia through decreases in fibrosis and apoptotic death and an increase in vascular density in the ischemic region.     

Intracoronary injection of granulocyte colony-stimulating factor ameliorates the progression of left ventricular remodeling after myocardial ischemia/reperfusion in rabbits.

BACKGROUND: Although granulocyte colony-stimulating factor (G-CSF) is known to prevent left ventricular (LV) remodeling after acute myocardial infarction (AMI), the best method of administration is unknown. METHODS AND RESULTS: A rabbit ischemia/reperfusion model was created and G-CSF was administered into the coronary artery immediately after reperfusion. The LV size and contraction were determined by echocardiography, and the extent of infarcted myocardium was measured by Masson-Trichrome staining. The benefits of intracoronary injection of G-CSF on LV remodeling were similar to subcutaneous injection. CONCLUSIONS: Direct intracoronary G-CSF injection may become a new therapy for AMI with lower adverse effects.     

骨髓干细胞动员促进兔缺血后肢血管新生的实验研究

目的观察干细胞动员剂动员骨髓干细胞后,促进兔缺血后肢血管新生的情况。方法切断股动脉及其分支,制作兔后肢缺血模型;实验组兔皮下注射重组人粒细胞集落刺激因子(rhG-CSF)动员兔自体干细胞释放和迁移至缺血组织;对照组给予生理盐水。术后4周,行腹主动脉造影观察侧支循环形成情况,并取内收肌和腓肠肌行病理切片HE染色,应用图像分析系统统计血管密度。结果实验组兔侧支循环血管数量和血管密度大于对照组(P<0.05),缺血状态得到改善。结论骨髓干细胞动员可促进血管新生,增加缺血下肢血液灌注,改善肢体缺血状态。     

经冠状动脉注入自体骨髓单个核细胞的临床研究

目的评价经冠状动脉内注射自体骨髓单个核细胞治疗心肌梗死患者的有效性。方法共有35例前壁心肌梗死患者人选本项前瞻性、非随机、开放试验（其中20例患者为细胞移植组,15例为对照组）。两组患者均接受标准的介入治疗和药物治疗,细胞移植组的20例患者同时接受自体骨髓单个核细胞移植。两组患者均接受3个月的临床随访及6min步行试验、超声心动图、心肌双核素和心脏核磁等检查。结果3个月的检查结果提示,细胞移植组患者的左室射血分数与常规治疗组相比有显著统计学意义。同时细胞移植组患者的室间隔中段室壁运动位移和左室收缩末容积也有明显改变,细胞移植组显著增加代谢可恢复心肌区占左室的比例。结论经冠状动脉注入自体骨髓单个核细胞可以促进心肌梗死患者寿窜功能恢复和心肌灌沣改善．     

Vascular endothelial growth factor-165 gene therapy promotes cardiomyogenesis in reperfused myocardial infarction

BACKGROUND: Vascular endothelial growth factor (VEGF)-165 promotes cardiomyogenesis in chronic myocardial ischemia and nonreperfused myocardial infarction (MI). It is unknown whether this effect is present in reperfused MI. We sought to investigate the effect of VEGF-165 gene therapy on cardiomyogenesis after reperfused MI. METHODS AND RESULTS: Twenty-four Yucatan minipigs underwent thoracotomy and a vascular clamp was placed in the left circumflex artery. Reperfusion was reestablished after 90 minutes, and VEGF-165 gene therapy or placebo was administered. A replication-deficient recombinant human adenovirus serotype 5 was used for gene transfer (Ad5-VEGF165). The same viral vector devoid of VEGF gene (Ad5-beta-galactosidase) was used as placebo. Two administration routes were tested, intramyocardial (IM) injection and circumflex intracoronary (IC) infusion. The pigs were assigned to one of the following groups: IM Ad5-VEGF165 (n = 6), IM Ad5-betaGal (n = 6), IC Ad5-VEGF165 (n = 6), and IC Ad5-betaGal (n = 6). All pigs received 5-bromo-2'-deoxyuridine (BrdU) 250 mg IV twice a week to label cells undergoing DNA replication. The hearts were explanted at 4 weeks. BrdU-labeled cardiomyocytes in the peri-infarct area were counted by a pathologist blinded to group assignment. The number of BrdU-labeled cardiomyocytes per million cells was 4-fold higher in the group receiving IM VEGF-165 (64 +/- 11.4) vs. IM placebo (16 +/- 10.6), P = 0.034. No difference in infarct size or ventricular function was observed between the groups. CONCLUSIONS: IM VEGF-165 gene therapy promotes cardiomyogenesis in reperfused MI. However, no benefit in infarct size or cardiac function was observed at 4 weeks. The origin of these cells remains unknown and needs to be determined.     

Macrophage colony-stimulating factor treatment after myocardial infarction attenuates left ventricular dysfunction by accelerating infarct repair.

OBJECTIVES: We aimed to determine the effects of macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF) treatment on both the repair process and ventricular function after myocardial infarction (MI). BACKGROUND: The M-CSF and G-CSF have multiple potential effects on cells involved in wound repair. METHODS: Myocardial infarction was induced by 45- or 90-min coronary occlusion and reperfusion in rats with or without subsequent injection of M-CSF (10(6) IU/kg/day) or G-CSF (50 microg/kg/day) for five days. We examined histology and messenger ribonucleic acid (mRNA), and assessed left ventricular function in situ using a conductance catheter. RESULTS: Five days after MI, M-CSF increased the number of ED-1-positive cells, mRNA levels of transforming growth factor-beta-1, collagen I and III, and collagen fibers within the infarct. Fourteen days after MI, induced by 45-min ischemia, left ventricular end-systolic elastance (Ees) was reduced (1,191 +/- 87 mm Hg/ml vs. 1,812 +/- 150 mm Hg/ml) and both isovolumic relaxation time constant (tau) (11.9 +/- 0.9 ms vs. 8.5 +/- 0.4 ms) and left ventricular end-diastolic volume (LVEDV) (0.225 +/- 0.014 ml vs. 0.172 +/- 0.011 ml) increased versus sham-operated rats. These alterations after MI were attenuated by M-CSF (Ees = 1,650 +/- 146, tau = 9.7 +/- 0.7, LVEDV = 0.199 +/- 0.012) but not by G-CSF. This beneficial effect of M-CSF on Ees was also detected in hearts with MI induced by 90-min ischemia. Furthermore, M-CSF increased collagen content within infarcts and reduced the proportion of thin collagen fibers 14 days after MI. The Ees significantly correlated with infarct collagen content. Nevertheless, neither M-CSF nor G-CSF modified infarct size. CONCLUSIONS: The M-CSF treatment attenuates deterioration of left ventricular function after MI by accelerating infarct repair.     

急性心肌梗死时G-CSF的抗心肌重构及对心功能改善的实验研究

目的探讨急性心肌梗死（AM I）时动员剂粒细胞集落刺激因子（G ranu locyte colony-stimu lating factor,G-CSF）抗心肌重构和功能保护作用。方法日本大耳白兔40只,随机分成两组,每组20只,均结扎冠状动脉前降支建立心肌梗死模型,动员剂组于模型建立后1 h给予G-CSF皮下注射连续7 d,对照组系建立心肌梗死模型后仅注射生理盐水。术前、术后24 h及术后4周做心脏超声检测心功能,4周后处死动物,取出心脏行组织病理学分析,测定两组梗死面积的大小、毛细血管密度以及观察纤维化的情况。结果动员剂组心功能各项指标在术后4周时均较对照组有明显的改善。HE染色显示对照组心肌纤维排列紊乱不规则,而动员剂组排列有序,梗死灶较对照组明显减小,且毛细血管密度也显著增加。胶原纤维明显少于对照组。结论急性心肌梗死时给予G-CSF可有效增加梗死区及周围毛细血管密度,缩小梗死面积,稳定心脏结构及显著改善心功能。     

BH3-only protein Bim is involved in myocardial injury induced by co-stress of ischemia and cold stress in rats

Objectives To investigate the effect of co-exposure of myocardial ischemia and cold stress on myocardial injury in rats and the relative mechanism.Methods Myocardial ischemia model was established by ligation of left coronary artery.SD rats were randomly allocated to 4 groups; sham+normal temperature(S group),sham+cold stress(SC group),myocardial ischemia+ normal temperature(Ⅰgroup), myocardial ischemia+cold stress(IC group).On the condition of 26℃,SC and IC groups were keeped in a 4℃artificial chamber for 8h(8;00-16:00) for 4 consecu- tive days.Car diac function was assessed by echocardiography;pathological change was analyzed by HE staining;myocardial infarct size was determined by TTC staining;Bim,Caspase-3 expression in myocardium was determined by western blotting.Results It was demonstrated that co-exposure of myocardial ischemia and cold stress could significantly make the cardiac muscle in abnormal shape,increase the infarct size and the expression of Bim and Caspase-3.Conclusions Co-exposure of myocardial ischemia and cold stress may aggravate the cardiac injury,pro- apoptosis protein Bim is involved.     

Peripheral blood stem cells transplantation in patients with heart failure after myocardial infarction:their efficiency and safety

Objective To compare the efficiency and safety of intracoronary transplantation of peripheral blood stem cells (PBSC) between elderly and younger patients with heart failure after myocardial infarction (MI). Methods Twenty-five patients with heart failure after MI were divided into aged group(≥60 years,n=13) and non-aged group(<60years,n=12)to receive intracoronary PBSC transplantation (PBSCT) following bone marrow cells mobilized by granulocyte colony-stimulating factor(G-CSF). Clinical data including coronary lesion characteristic, left ventricular shape,infarct region area and cardiac function, as well as adverse side effects between the two groups were compared. Left ventricular function was evaluated before and 6 months after the treatment by single photon emission computed tomography(SPECT). Results At 6 months, the left ventricular ejection fraction (LVEF) and 6 minute walk test (6MWT) distance increased, while the left ventricular diastolic diameter (LVDd) decreased significantly in both groups. There were no significant difference between the two groups in absolute change in the cardiac function parameters. Conclusions The present study demonstrated that autologous intracoronary PBSCT might be safe and feasible for both old and younger patients with heart failure after MI and left ventricular function is significantly improved.(J Geriatr Cardiol 2007;4:233-237.)     

Effects of intracoronary thrombolysis on infarct size and left ventricular function in patients with anterior myocardial infarction--enzymatic, electrocardiographic, radionuclide and hemodynamic evaluations

The influence of the duration of ischemia on infarct size and left ventricular function (LV) was assessed in 30 patients with a first anterior myocardial infarction (MI) and intracoronary thrombolysis (ICTL) on admission. The occlusion time of the left anterior descending coronary artery (LAD) was 4 hours or less in 11 patients (group I), 4-10 hours in 11 (group II) and 10 hours or more in eight (group III). Serial measurements of serum creatine kinase-MB were carried out during the acute phase. Four weeks after the procedure, electrocardiographic pathological Q waves on 34-lead precordial mapping were scored, viable left ventricular myocardial volume and the ratio of infarcted to total left ventricular myocardial volume was estimated by myocardial emission computed tomography (ECT) with thallium-201. In the acute phase enzymatic estimation of infarct size showed a significant difference between group I and the other two groups but not between groups II and III; there were no significant differences in the degree of left ventricular asynergy among the three groups. In the chronic phase infarct sizes evaluated by both Q wave mapping and ECT were smaller in group I than those in group II, which were smaller than those in group III; there were significant differences in the degree of LV asynergy among the three groups (group I less than II less than III). LV function was nearly normal in group I, moderately impaired in group II, but severely depressed in group III 4 weeks later. The present study indicates that infarct size extends and LV function deteriorates with the duration of occlusion of the LAD and that not only early (less than or equal to 4 hours) but also later (4-10 hours) reperfusion is beneficial to prevent the extension of MI and deterioration of LV function in patients with anterior MI.