流式细胞术对冠心病患者血小板表面活化标志蛋白的研究

目的 :探讨流式细胞术 (FCM)测定的血小板活化指标与冠心病 (CHD)的关系。方法 :利用 FCM和单克隆抗体测定 31例稳定型心绞痛 (SAP组 )、65例不稳定型心绞痛 (UAP组 )和 2 5例急性心肌梗死 (AMI组 )患者的外周血中血小板糖蛋白 CD62 P、CD63和凝血酶敏感蛋白 (TSP)的阳性表达率 ,并与 39例正常人作对照。结果 :FCM可简单、迅速地检测血小板的活化功能 ,CHD患者 CD62 P、CD63和 TSP的阳性表达率均显著高于对照组 (P <0 .0 5)。在 CHD患者中 ,UAP组和AMI组的 CD62 P、CD63和 TSP的表达率均显著高于 SAP组 (P <0 .0 5) ,AMI组又高于 UAP组。结论 :CHD患者血小板活化是导致血小板功能亢进的原因 ,并参与了 CHD尤其是 UAP和AMI的病理过程 ;FCM是测定血小板活化功能既准确又可靠的方法之一。     

冠心病患者白细胞变形能力和粘附功能及细胞粘附分子表达的变化

为探讨白细胞变形能力、粘附功能和细胞粘附分子与冠心病的关系，检测了188例冠心病患者和68例健康人外周血白细胞滤过指数、粘附率、白细胞CD18表达和血清可溶性细胞间粘附分子-1浓度变化。结果发现，冠心病病人白细胞滤过指数、粘附率、白细胞CD18表达及可溶性细胞间粘附分子-1浓度均明显增高，与对照组比较差异有极显著性意义（P＜0．001）。急性心肌梗塞病人各指标增高较不稳定心绞痛和陈旧性心肌梗塞更明显（P＜0．001）、冠心病病人白细胞滤过指数、粘附率与白细胞CD18表达和可溶性细胞间粘附分子-1浓渡呈正相关（r=0．679～0．764，P＜0．001），白细胞滤过指数与粘附率呈正相关（r=0.663，P＜0．001）。提示白细胞变形能力降低，粘附功能和CD18表达及可溶性细胞间粘附分子-1浓度增高，参与了冠心病的发生，且与病情变化有关。     

冠状动脉支架术对冠心病患者血小板活化功能的影响

目的探讨冠心病患者行冠状动脉内支架置入术前后血小板活化指标的变化,了解冠心病不同临床类型支架置入数与血小板活化指标之间的关系。方法利用流式细胞术和单克隆抗体测定48例稳定型心绞痛、45例不稳定型心绞痛患者与37例急性心肌梗死患者外周血中血小板膜糖蛋白CD62p、CD63和凝血酶敏感蛋白的阳性表达率,并与45例冠状动脉造影正常者作对照分析。结果稳定型心绞痛患者、不稳定型心绞痛患者和急性心肌梗死患者支架置入后CD62p、CD63和凝血酶敏感蛋白的阳性表达率均显著高于支架置入前(P<0.01);不稳定型心绞痛组和急性心肌梗死组治疗前亦高于对照组(P<0.01),而稳定型心绞痛组治疗前与对照组比较差异无显著性(P>0.05)。稳定型心绞痛组和不稳定型心绞痛组CD62p、CD63和凝血酶敏感蛋白的阳性表达率与支架置入个数有关,置入支架越多阳性表达率越高。结论不稳定型心绞痛患者及急性心肌梗死患者存在血小板高活化状态、动脉粥样硬化斑块破裂以及急性血栓形成。支架置入术对冠状动脉内皮的损伤加强了血小板的活化,增加了血栓形成的风险。     

急性冠状动脉综合征支架置入与血小板活化的临床研究

目的探讨急性冠状动脉综合征(acute coronary syndrome,ACS)患者行冠状动脉(冠脉)内支架置入术前、后血小板活化指标的变化。方法利用流式细胞术(flowcytometry,FCM)和单克隆抗体测定45例不稳定型心绞痛(unstable angina pectoris,UAP)与37例急性心肌梗死(acute myocardial in-farction,AMI)患者外周血中血小板膜糖蛋白CD62p,CD63和凝血酶敏感蛋白(thrombin-sensitive protein,TSP)的阳性表达率,并与45例冠脉造影正常者相对照。结果FCM可简单、迅速地检测血小板的活化功能。ACS患者支架置入后CD62p,CD63和TSP的阳性表达率均显著高于支架置入前;ACS组治疗前亦高于对照组。结论急性冠脉综合征伴随血小板活化,介入治疗进一步加强血小板的活化。     

冠心病患者外周血白细胞表面粘附分子的表达

目的　目前认为炎症可能在冠心病发病及恶化过程中起重要的作用。本研究通过测定冠心病患者外周血中性粒细胞和单核细胞表面CD11b、CD18的表达 ,探讨炎症与冠心病的关系。方法　选择 5 4例冠心病患者 ,其中急性心肌梗死 2 5例 ,不稳定心绞痛患者 2 9例。根据不稳定心绞痛患者病情的严重程度将其按Braunwald分级分为三组 :第一组 (9例 ,BraunwaldⅠ级 ) ;第二组 (8例BraunwaldⅡ级 ) ;第三组 (12例BraunwaldⅢ级 )。选择 12例健康人为正常对照组。采用流式细胞术分析外周血中性粒细胞和单核细胞表面粘附分子CD11b、CD18的表达。结果　冠心病患者外周血中性粒细胞和单核细胞表面CD11b、CD18的表达较正常对照组显著升高 (P <0 0 0 1) ;不稳定心绞痛患者由第一组到第三组外周血中性粒细胞和单核细胞表面CD11b、CD18的表达是逐渐升高的 ,且第一组与第三组有统计学意义 (P <0 0 5 )。结论　冠心病患者外周血白细胞是激活的 ;随着不稳定心绞痛病情的加重 ,外周血白细胞活性也是增加的 ,白细胞活性状态与冠脉缺血的严重程度正相关     

黏附分子及CD40配体与急性心肌梗死的关系

目的观察青年急性心肌梗死患者淋巴细胞的血管间黏附分子、淋巴细胞黏附分子(VCAM-1及ICAM-1)及CD40配体(CD40L)的表达,探讨其急性心肌梗死炎症免疫学发病机制。方法将年龄≤45岁,与年龄>45岁急性心肌梗死患者上述指标比较,体检正常者作为对照。用流式细胞仪检测淋巴细胞VCAM-1、ICAM-1及CD40L阳性表达率。结果≥45岁组VCAM-1、ICAM-1及CD40L明显高于正常对照组(P<0.05),但与老年心肌梗死组对比差异无显著意义(P>0.05)。≤45岁心肌梗死组中VCAM-1、ICAM-1与CD40L显著相关。结论VCAM-1、ICAM-1及CD40L的高表达是急性心肌梗死发生和发展的重要炎症免疫学机制之一。     

黏附分子CD56、CD44、CD54、CD11a在急性髓系白血病骨髓中的表达及意义

目的:探讨黏附分子CD56、CD44、CD54、CD11a在急性髓系白血病(AML)骨髓中的表达情况及临床意义。方法:流式细胞仪检测57例AML患者和20例正常对照者骨髓单个核细胞表面CD56、CD44、CD54、CD11a的表达水平,分析其与AML患者白细胞计数、白细胞淤滞及早期病死率的关系。结果:1CD56仅在AML组表达(AML组表达率为35.1%,正常对照组0,P0.05),其在AML高白细胞(HAML)组的表达率(53.3%)高于AML非高白细胞(NHAML)组(28.6%),白细胞淤滞组(62.5%)高于无白细胞淤滞组(28.9%)(P0.05);2AML患者骨髓单个核细胞表面CD44的平均荧光强度在HAML组显著高于NHAML组(P0.05),其表达与AML患者外周血白细胞计数呈正相关(r=0.446,P0.01)。CD56、CD54、CD11a在HAML组与NHAML组、无白细胞淤滞组与白细胞淤滞组的平均荧光强度均差异无统计学意义(P0.05)。3AML患者中HAML组、白细胞淤滞组患者的早期病死率(33.3%、25.0%)分别明显高于NHAML组、无白细胞淤滞组(0、0)。结论:CD56在HAML患者和白细胞淤滞患者有更高的表达率,有可能是AML患者预后不良的因素之一;CD44在AML患者骨髓中的表达水平与外周血白细胞计数呈正相关,可能参与HAML的发生。CD54、CD11a与HAML及白细胞淤滞的关系不十分密切。     

急性肺损伤不同时期白细胞粘附分子的表达及其意义

目的探讨白细胞粘附分子在急性肺损伤(ALI)/急性呼吸窘迫综合征(ARDS)发病机制中的作用。方法采用流式细胞术,用单克隆抗体定量测定2004年6月至2005年12月华中科技大学同济医学院附属同济医院重症监护病房的26例ALI患者、18例ARDS患者和15名健康人外周血中白细胞粘附分子CD11a、CD11b和CD18的阳性表达率,并比较治愈组与死亡组患者白细胞粘附分子CD11a、CD11b和CD18的阳性表达率。结果ALI组和ARDS组外周血中性粒细胞和单核细胞表面的CD11a、CD11b和CD18明显高于健康对照组(P<0.01),ARDS组中性粒细胞、单核细胞和淋巴细胞表面的CD11a、CD11b和CD18,明显高于ALI组(P<0.05);死亡组患者中性粒细胞表面的CD11a、CD11b和CD18明显高于治愈组(P<0.05)。结论ALI患者通过中性粒细胞和单核细胞CD11a/CD18、CD11b/CD18的表达上调,ARDS患者通过中性粒细胞、单核细胞和淋巴细胞表面CD11a/CD18、CD11b/CD18的表达上调,参与各自疾病的病理发展过程。中性粒细胞CD11a/CD18、CD11b/CD18的表达水平与预后密切相关。     

冠心病患者PTCA手术前、后CD11b/CD18的表达及临床意义

探讨不同类型 CHD患者白细胞粘附分子的变化和 PTCA对白细胞粘附分子表达的影响。选择行冠状动脉造影 （CA）和 PTCA术的患者 2 7例 ,将其分为 SAP组、UAP组及正常对照组。分别检测 CA或 PTCA术前、术后 6h,2 4h,48h的白细胞计数及 CD11b/ CD18在单核细胞和中性粒细胞 （PMN）膜上的表达。结果 :1CHD患者血液中单核细胞、PMN的 CD11b/ CD18表达较健康对照组均显著增加 （P<0 .0 1） ,其中 U AP组最为明显。 2 PTCA术后白细胞计数和单核细胞 CD11b/ CD18表达与术前无明显差异 ,而 PMN膜 CD11b/ CD18表达在 6 h开始升高 （P<0 .0 1） ,48h升高尤为显著。而 CA术前后各项检测指标均无差异。结论 :CHD患者 PMN、单核细胞膜上 CD11b/CD18的表达明显增加 ,粘附性增强 ,其增加程度与心肌缺血状态有关 ;PTCA术后 PMN膜 CD11/ CD18表达的上调 ,可能是冠脉再狭窄的原因之一。     

冠心病患者中性粒细胞和单核细胞CD11b/CD18表达的研究

目的 :探讨不同类型冠心病患者中性粒细胞和单核细胞膜 CD11b/CD18表达的变化。方法 :选择经冠状动脉造影确诊的 49例心绞痛患者 ,30例急性心肌梗死患者和 2 0例正常人 ,用流式细胞仪直接免疫荧光法检测中性粒细胞和单核细胞膜 CD11b/CD18表达。结果 :冠心病患者中性粒细胞和单核细胞膜 CD11b/CD18表达较正常对照组均显著增加 （P<0 .0 1） ;不稳定性心绞痛和急性心肌梗死患者中性粒细胞和单核细胞膜 CD11b/CD18表达显著高于稳定性心绞痛患者 （P<0 .0 1）。与正常对照组比较 ,心绞痛患者组中性粒细胞和单核细胞计数无变化 （P>0 .0 5 ） ,而急性心肌梗死组明显增加 （P<0 .0 1）。急性心肌梗死患者中性粒细胞和单核细胞膜 CD11b/CD18表达与梗死范围无关。结论 :冠心病患者中性粒细胞和单核细胞膜 CD11b/CD18表达明显增加 ,其增加程度与心肌缺血的类型有关。     

白细胞变形能力和粘附功能与急性心肌梗塞病情相关性

白细胞变形能力和粘附功能与急性心肌梗塞病情相关性刘成玉１曲彦２纪新强３滕青４谭润鸾１（１．青岛医学院诊断学教研室２６６０２１２．青岛市市立医院２６６０２１３．青岛医学院预防医学教研室２６６０２１４．青岛市浮山医院２６６０７１）ＴｈｅＣｏｒｅｌａｔｉｏ...     

血清淀粉样蛋白A1在急性心梗中的早期诊断及预后

[摘要] 目的：本研究探讨SAA1表达水平与急性心肌梗死及其预后的相关性,以及急性心肌梗死患者、不稳定心绞痛患者、稳定性心绞痛患者与健康人群的差异性表达。方法：选取2016年10月至2018年7月于我院行冠状动脉造影术的110例患者和健康体检的30例患者,作为研究对象;其中急性心肌梗死组（AMI组）50人,不稳定心绞痛组（UA组）32人,稳定性心绞痛组（SAP组）28人,正常组（CON组）30人;其中急性心肌梗死组分为发病当天（AMI0组）及入院7天组（AMI7组）,对比各组间SAA1指标的差异性。并收集患者的一般资料及相关化验检查。Pearson相关分析方法分析HDL-C及BNP水平与急性心梗组SAA1水平的相关性;同时初步探究SAA1水平与心梗后心功能不全发生风险的相关性。结果：AMI组SAA1水平明显高于其他三组（UAP、SAP、CON组）,两两比较均具有统计学意义（P=0.000）;UA组SAA1水平明显高于CON组,且高于SAP组,两两比较均有统计学差异（P=0.047,P=0.009）; SAP组与CON组差异无统计学意义（P=0.507）。 BNP升高水平同AMI组中SAA1水平具有明确正相关（r=0.421,P=0.045）;HDL-C水平同AMI组中SAA1水平具有明确负相关（r=-0.445,P=0.033）;而LDL-C及cTnI同AMI组中SAA1水平无统计学差异（r=0.015,P=0.945;r=-0.171,P=0.436）。AMI0组SAA1水平明显高于AMI7组,差异存在统计学意义（P=0.002）。结论：SAA1蛋白在急性心肌梗死、不稳定心绞痛、稳定性心绞痛与健康人群中存在明显差异。在急性心梗组中SAA1升高水平与BNP呈正相关,提示心梗后心衰风险升高。 SAA1蛋白在急性心肌梗死中发病当天及7天后存在的明显差异。     

Aminobenzoic acid hydrazide, a myeloperoxidase inhibitor, alters the adhesive properties of neutrophils isolated from acute myocardial infarction patients

Acute myocardial infarction (AMI) is associated with vascular inflammation, including activation and adherence of neutrophils to vascular endothelial cells via CD11b/CD18 intercellular adhesion molecule interactions. Myeloperoxidase (MPO) induces CD11b surface expression in polymorphonuclear neutrophils (PMNs); however, its role in regulating adhesion in AMI is not well characterized. This study investigates the effects of aminobenzoic acid hydrazide (ABAH), an inhibitor of MPO, antibodies specific for CD11b, on the adhesion of PMNs isolated from AMI patients to endothelial cells. Human neutrophils were isolated from the peripheral blood of 20 patients with AMI or 20 healthy participants as control using Percoll density gradient centrifugation. The major biochemical indicators were detected with different biochemical analyses. The effects of ABAH and anti-CD11b antibodies on neutrophil adhesion to endothelial cell were measured using adhesion assays in vitro. The adhesion rate was significantly higher for neutrophils isolated from AMI patients than healthy individuals (P < 0.001). ABAH significantly inhibited MPO activity in PMNs isolated from AMI patients. Neutrophil adhesion was significantly reduced upon treatment with 10 and 20 μM ABAH in a dose-dependent manner. Treatment with anti-CD11b antibodies also significantly reduced neutrophil adhesion in comparison with the untreated control group (P < 0.001). Thus, both ABAH and anti-CD11b antibodies reduced PMN adhesion. Further studies are necessary to determine whether MPO enhances neutrophil adhesion to endothelial cells in AMI patients through the upregulation of CD11b expression on the surface of neutrophils, which is abrogated by ABAH.     

Increased plasma level of soluble E-selectin in acute myocardial infarction

BACKGROUND: E-selectin, also known as endothelial cell leukocyte adhesion molecule-1, is a member of the selectin family of adhesion molecules and is expressed on vascular endothelial cells in inflammatory reactions. The induction of surface E-selectin expression by endothelial cells is considered a marker of activation. METHODS AND RESULTS: We examined the plasma soluble E-selectin (sE-selectin) level in 41 patients within 6 hours after the onset of acute myocardial infarction (AMI) and in 37 patients with stable exertional angina and 27 control patients. Blood samples were obtained on admission, after reperfusion therapy, and at 4 hours, 8 hours, 12 hours, 24 hours, 48 hours, 3 days, 5 days, 1 week, and 2 weeks after admission in the AMI group. In this group, 21 patients had a history of prodromal unstable angina before infarction and 20 had sudden onset of infarction. The plasma sE-selectin level (ng/mL) on admission was higher in the AMI group than in the stable exertional angina group and control group (38.5 +/- 3.1 vs 28.5 +/- 1.5, P <.01, 26.0 +/- 1.8, P <.01, respectively). In addition, plasma sE-selectin levels were higher in the patients with AMI with prodromal unstable angina than in those with a sudden onset of infarction on admission (44.7 +/- 5.4 vs 32.0 +/- 2.1, P <.05). The plasma sE-selectin level decreased slowly during the chronic phase both in patients with AMI with prodromal unstable angina (from 44.7 +/- 5.4 to 33.8 +/- 3.4, P <.01) and those with a sudden onset of infarction (from 32.0 +/- 2.1 to 24.9 +/- 2.4, P <.01). CONCLUSIONS: These results suggest that an increase of sE-selectin may reflect enhanced endothelial cell activation in patients with AMI. The higher sE-selectin level in patients with AMI with prodromal unstable angina may have been associated with repeated episodes of myocardial ischemia and reperfusion.     

血红素氧化酶-1在老年人急性心肌梗死患者中的表达

目的　观察血红素氧化酶- 1(HO -1)在老年急性心肌梗死(AMI)患者中的表达。方法　选择70岁以上确诊AMI的老年人35例(AMI组)及经冠状动脉造影确诊的无心肌梗死冠心病患者4 0例(冠心病组) ,并选择冠状动脉造影正常的4 0例患者作为对照组。利用Westernblot方法对研究对象外周血单个核细胞中HO- 1的表达进行定量分析。结果　老年冠心病患者HO- 1表达水平高于对照组,AMI组患者HO -1表达明显高于冠心病组患者(P <0 .0 1)。结论　老年人AMI时,HO -1表达水平明显升高。     

Enhanced expression of platelet CD40-ligand by in vitro lipopolysaccharide-challenge in patients with ventricular fibrillation complicating acute myocardial infarction

BACKGROUND: Acute myocardial infarction can be complicated by ventricular arrhythmias due to electrophysiological changes in the ischemic myocardium, but the exact predisposing factors causing ventricular fibrillation during myocardial infarction still remain unclear. A role of inflammatory stimulation on platelets as a potential risk factor for ventricular fibrillation during acute myocardial infarction has not been described yet. METHODS AND RESULTS: Whole blood samples of 21 patients with a history of acute myocardial infarction (AMI) and ventricular fibrillation (VF) were incubated with lipopolysaccharide (LPS). As a control group, we studied 19 patients without VF during AMI. CD40-ligand and CD62P expression on platelets and tissue factor binding on monocytes were measured by flow cytometry. Platelet-monocyte aggregates were measured by CD41 expression on platelets adherent to monocytes. Soluble CD40-ligand plasma levels were measured with an ELISA. Without LPS, no significant difference between the patient groups concerning CD40L expression on platelets was observed, but plasma levels of soluble CD40L were significantly higher in patients with a history of AMI with VF. After LPS stimulation, patients with a history of VF showed a significantly increased expression of CD40L in comparison to the patients without ventricular fibrillation, based on a significantly higher increase of CD40L expression. CD62P expression on platelets was significantly increased in patients with a history of VF. CONCLUSIONS: Patients with a history of VF complicating AMI show an enhanced expression of CD40L on platelets after in vitro lipopolysaccharide-challenge with an enhanced platelet activation.     

老年急性心肌梗死患者中性粒细胞黏附分子的表达和溶栓治疗的影响

目的观察老年急性心肌梗死患者中性粒细胞表面黏附分子L-selectin和CD11b的表达以及溶栓治疗对其影响. 方法用免疫荧光技术和流式细胞术测定30例正常对照组和32例老年急性心肌梗死患者溶栓前后中性粒细胞表面黏附分子L-selectin和CD11b的表达. 结果与对照组相比,急性心肌梗死患者中性粒细胞L-selectin的表达下降47.3%（P＜0.01）,而CD11b的表达升高145.5%（P＜0.01）.溶栓治疗前后中性粒细胞L-selectin和CD11b的表达无明显变化. 结论老年急性心肌梗死患者中性粒细胞L-selectin表达下调,CD11b表达上调,提示中性粒细胞被激活.溶栓治疗对中性粒细胞表面黏附分子的表达无影响.     

Increased Expression of Neutrophil and Monocyte Adhesion Molecules LFA-1 and Mac-1 and Their Ligand ICAM-1 and VLA-4 Throughout the Acute Phase of Myocardial Infarction: Possible Implications for Leukocyte Aggregation and Microvascular Plugging

Objectives. This study sought to evaluate expression of adhesion molecules on neutrophils and monocytes throughout the acute phase of myocardial infarction.Background. Neutrophil and monocyte counts increase within days from onset of acute myocardial infarction. Because leukocytes are recruited to the involved myocardial region, we postulated that these activated cells would display an increased expression of adhesion molecules necessary for effective endothelial transmigration.Methods. We measured the expression of neutrophil and monocyte lymphocyte function associated antigen-1 (LFA-1), Mac-1, very late after activation antigen-4 (VLA-4) and intercellular adhesion molecule-1 (ICAM-1) by flow cytometry throughout the acute phase of acute myocardial infarction in 25 patients and 10 age-matched control subjects.Results. Expression of Mac-1 on neutrophils increased significantly, whereas no expression of VLA-4 and ICAM-1 was detected. The expression of LFA-1, Mac-1, VLA-4 and ICAM-1 on the monocyte cell membrane in patients with an acute myocardial infarction was increased compared with that in control subjects by 22% (on day 7), 67%, 13% and 44% (all on day 4), respectively (all p < 0.001). Elevated density of monocyte-specific CD14 in the AMI versus the control group was also shown (30%, p < 0.001).Conclusions. Increased expression of neutrophil and monocyte adhesion molecules may contribute to their adhesion to endothelium in the ischemic territory. This adhesion could feasibly precipitate vasoconstriction or add a local thrombotic effect due to tissue factor expression secondary to Mac-1 engagement. In addition, the manifestation of increased density of LFA-1 and Mac-1 by activated leukocytes with monocytes also expressing ICAM-1 suggests that leukocytes may form microaggregates that could cause microvascular plugging. This mechanism may facilitate the occurrence of the “no-reflow” phenomenon or slow coronary filling after acute myocardial infarction.     

SHH信号通路激活对急性心肌梗死大鼠缺血心肌血管再生的作用

目的 探讨SHH(sonic hedgehog)信号通路激活对急性心肌梗死(AMI)大鼠缺血心肌血管再生作用及机制。方法 雄性成年SD大鼠80只,体质量（150~200）g采用结扎大鼠左前降支的方法制备AMI大鼠模型,随机分为单纯心肌梗死(AMI)组,外源性重组人SHH蛋白（rhSHH）处理组,SHH信号通路抑制剂Cyclopamine(CYC)处理组,连续处理7 d后,利用VIII因子免疫组织化学染色测定rhSHH对AMI大鼠缺血心肌微血管密度的影响;TTC染色观察各组心肌梗死面积;ELISA和RT-PCR方法测定AMI大鼠缺血心肌促血管再生相关的指标血管内皮生长因子(VEGF),碱性成纤维细胞生长因子(bFGF)及血管生成素(Ang)-1的血清和mRNA表达;Western blot检测各组SHH信号通路相关蛋白SHH,SMO,Gli-1的蛋白表达。结果 与AMI组相比,rhSHH处理后缺血心肌微血管密度显著增加（P<0.05）,心肌梗死面积减小（P<0.01）,血管生长因子VEGF,bFGF,Ang-1的血清水平和mRNA表达显著增加（P<0.01）,心肌梗死边缘区SHH信号通路下游靶分子(SHH,SMO,Gli-1)的蛋白表达显著增加（P<0.05）;这种影响可以被SHH信号通路抑制剂Cyclopamine所逆转（P<0.01）。结论 激活SHH通路可增加缺血心肌血管生长因子VEGF,bFGF,Ang-1的表达,促进急性心肌梗死大鼠的血管再生。