造影增强实时三维超声心动图定量评价心肌梗死犬心肌灌注及其局部收缩功能

目的应用造影增强实时三维超声心动图(CE-RT3DE)定量评价心肌梗死犬心肌灌注及其局部收缩功能。方法建立犬急性心肌梗死(冠脉结扎180min,再灌注30min)模型。分别于基础状态、冠脉结扎180min及再灌注30min时行CE-RT3DE,获取其RT-3DE容积数据库;脱机后根据心尖长轴8平面法勾画舒张末期左室心肌灌注缺损区体积(VPMD)和室壁运动异常区体积(VWMA)。取出心脏后,用伊文思蓝(Evansblue,EB)和TTC染色确定危险心肌和梗死心肌,先后剥离并测量危险心肌体积(VAREVANS)和梗死心肌体积(IVTTC)。结果冠脉结扎180min时VWMA[(15.31±3.06)ml]明显大于VPMD[(10.31±2.01)ml](P<0.001)。再灌注30min时VWMA[(14.97±2.93)ml]无明显变化(P=0.64);而VPMD[(4.23±0.80)ml]明显减小(P<0.001)。CE-RT3DE所测危险心肌体积[VARCE-TR3DE,(10.31±2.01)ml]与EB染色结果[VAREVANS,(10.61±2.02)ml]无明显差异(P=0.16)且两者显著相关(r=0.94);CE-RT3DE所测梗死心肌体积[IVCE-RT3DE,(4.23±0.80)ml]与TTC染色结果[IVTTC,(4.42±0.80)ml]无明显差异(P=0.07)且两者显著相关(r=0.92)。结论CE-RT3DE可准确评价心肌梗死犬的心肌灌注及其局部收缩功能,有望为临床识别及定量评价梗死心肌提供一项有效手段。     

造影增强实时三维超声心动图定量评价心肌顿抑犬的心肌灌注及其局部收缩功能

目的应用造影增强实时三维超声心动图(CERT3DE)定量评价心肌顿抑犬的心肌灌注及其局部收缩功能。方法建立犬心肌顿抑模型[冠状动脉(冠脉)结扎15min再灌注30min]。分别于基础状态、冠脉结扎15min及再灌注30min时行CERT3DE,获取其RT3DE容积数据库;脱机后根据心尖长轴观八平面法勾画舒张末期左室心肌灌注缺损区体积(VPMD)和室壁运动异常区体积(VWMA)。取出心脏,用伊文思蓝和三苯基四氮唑(TTC)染色,确定危险心肌及有无梗死心肌,剥离并测量危险心肌体积(VAREVANS)。结果冠脉结扎15min时:VWMA为(13.6±2.2)ml,VPMD为(9.0±1.4)ml,差异有显著性意义(P<0.001);再灌注30min时:VWMA为(13.0±1.9)ml,而VPMD为零,差异有显著性意义(P<0.001)。CERT3DE所测VARCERT3DE[(9.0±1.4)ml]与伊文思蓝染色结果VAREVANS[(9.2±1.5)ml]差异无显著性意义(P=0.16)且两者显著相关(r=0.92);CERT3DE所测顿抑心肌体积为(13.0±1.9)ml,TTC染色证实该区心肌无明显坏死。结论CERT3DE可准确评价心肌顿抑犬的心肌灌注及其局部收缩功能,有望为临床识别及定量评价顿抑心肌提供一项有效手段。     

心肌造影实时三维超声心动图定量评价缺血心肌的准确性研究

目的　评价心肌造影实时三维超声心动图(RT 3DE)测量缺血心肌质量的可重复性与准确性。方法　对21只健康杂种犬行开胸手术,结扎冠状动脉分支造成心肌缺血,分别于结扎前后进行 RT 3DE检查。静脉注射氟烷造影剂进行心肌造影,勾划相应的缺血心肌体积并计算其质量。结果　心肌造影 RT 3DE所测缺血心肌质量为(12.3±5.3)g,与伊文思蓝染色后离体测量结果显著相关( r=0.96)。两种测量方法的组间及组内差异比较具有高度的一致性。结论　心肌造影RT 3DE能准确计算犬缺血心肌质量,有望为临床定量评价冠心病患者心肌缺血提供一项新的手段。     

实时三维超声心动图声学造影定量评价左室质量的准确性研究

目的　评价实时三维超声心动图声学造影 (CE- RT3DE)测量左室心肌质量的准确性。方法　研究对象包括杂种犬 2 7只。经静脉注射氟碳造影剂后进行实时三维超声心动图检查 (Philips Sonos 75 0 0 ) ,勾划相应的左室心肌体积 ,乘以犬心肌密度计算质量。结果　 CE- RT3DE所测左室质量为 (5 7.9± 9.8) g,犬离体左室的实际质量为 (5 8.2± 10 .0 ) g,两种方法测量结果明显相关(r=0 .98)。结论　 CE- RT3DE能为临床评价左室质量提供一项准确可靠的新方法。     

声学造影实时三维超声心动图评价犬急性冠状动脉闭塞的侧支循环

目的 应用声学造影实时三维超声心动图评价急性冠状动脉闭塞犬的侧支循环.方法 结扎12只健康杂种犬左前降支,分别于结扎前、结扎后即刻、结扎后30 min及结扎后180 min时行心肌声学造影观察,并计算供血区心肌重量. 结果左前降支结扎后所有实验犬均有不同程度的侧支循环建立.结扎后30 min,侧支循环供血区心肌重量为(9.65±2.90)g;结扎后180 min,侧支循环供血区心肌重量为(12.58±3.98)g;二者之间差异有统计学意义. 结论 应用声学造影实时三维超声心动图可以很好地显示冠状动脉侧支循环的形成,并获得全面准确的侧支循环区心肌重量.     

心肌灌注声学造影与切面超声观察室壁运动在估计实验性心肌缺血梗塞范围上的应用

本文报告了用切面超声观察8只犬左前降支结扎后左室短轴切面上室壁矛盾运动区或无运动区(ADA)和室壁收缩期变薄区(WST)以及双氧水心肌灌注声学造影时的超声心动图造影缺损区(ECD)的部位和范围,并与氧化三苯四唑(TTC)染色所示心肌梗塞部位和范围进行比较。     

实时三维超声心动图评价多巴酚丁胺对心肌顿抑和梗死犬左心室局部径向距离的影响

目的应用实时三维超声心动图(RT-3DE)定量评价多巴酚丁胺对心肌顿抑犬和心肌梗死犬左心室局部径向距离的作用。方法建立犬的心肌顿抑[冠状动脉(冠脉)结扎15 min,再灌注30 min]和急性心肌梗死(冠脉结扎180 min,再灌注30 min)模型。于冠脉结扎前和冠脉结扎-再灌注后,用微量输液泵经股静脉输注多巴酚丁胺5及10μg.kg-1.min-1,每一剂量持续5 min。应用RT-3DE获取实验犬静息状态及输注多巴酚丁胺10μg.kg-1.min-1后RT-3DE全容积数据库。脱机后,根据心尖长轴观8平面法重建收缩末期左室立体几何形状;以二尖瓣环中点至左室心尖部心内膜的连线为中心轴,将左室等分成与中心轴垂直的1.0 cm厚互相平行的短轴平面,从中选取室壁运动异常(WMA)面积最大者作为研究平面;在此平面上,以轴心与左室后壁连线所在位置为0°,逆时针每隔20°测量心内膜至轴心的距离(即径向距离R,共可测得18个值)。将冠脉结扎-再灌注后两组实验犬输注多巴酚丁胺前、后的平均R值与冠脉结扎前(设为基础状态)输注多巴酚丁胺前、后的相应R值进行比较。结果静息状态下,心肌顿抑组和心肌梗死组中所选研究平面结扎冠脉供血区平均R值均明显增大(均P<0.001)。输注多巴酚丁胺后,心肌顿抑组中上述异常增大的平均R值均明显减小(均P<0.001),但未恢复至基础状态水平(均P<0.05);心肌梗死组中上述异常增大的平均R值均无明显改变(均P>0.05)。结论通过应用RT-3DE分析输注多巴酚丁胺前、后左室局部径向距离的变化,可以识别心肌顿抑和心肌梗死。RT-3DE有望为临床定量评价左室局部几何形状提供一项有效手段。     

实时三维心肌超声造影评估心肌灌注缺损的实验研究

目的　探讨实时三维超声心动图 (RT 3DE)结合心肌超声造影评估心肌灌注缺损区的可行性和准确性。方法　 1 3只杂种犬分别结扎左前降支 ( 6只 )或回旋支 ( 7只 ) ,经静脉注射氟烷微泡造影剂 ,应用RT 3DE显示并检测心肌灌注缺损区。心脏摘出后 ,经冠状动脉口注射伊文思蓝染料确定危险区心肌 ,以解剖方法直接测量心肌的质量作为判断标准。结果　①冠状动脉结扎前实时三维成像测定左心室质量与离体左心室心肌实测质量差异无显著性意义 ,且密切相关 (P >0 .0 5 ,r =0 .99)。②结扎左前降支组RT 3DE测量的左心室心肌总质量与心肌标本实测总质量之间比较差异无显著性意义 (P >0 .0 5 ) ;RT 3DE检测的灌注缺损区心肌质量与心肌标本实测危险区心肌质量之间比较 ,差异也无显著性意义 (P >0 .0 5 )。③结扎回旋支组RT 3DE与心肌标本测量的左心室质量、灌注缺损区心肌质量比较 ,二者差异均无显著性意义 (均P >0 .0 5 )。④观察冠状动脉结扎后所有动物心脏 ,RT 3DE测定的左心室总质量与心肌标本比较 ,二者差异无显著性意义 ( P >0 .0 5 ) ,且存在显著相关关系 (r =0 .99)。RT 3DE测量的灌注缺损区心肌质量与心肌标本对照 ,同样差异无显著性意义 (P>0 .0 5 ) ,且二者测量的结果显著相关 (r =0 .96)。结论　实时三维超     

心肌声学造影评价硝酸甘油对犬心肌缺血再灌注损伤的延迟保护作用

目的　探讨心肌声学造影 (myocardial contrastechocardiography,MCE)技术评价硝酸甘油对犬心肌缺血再灌注损伤的延迟保护作用的价值。方法　 12只健康成年杂种犬随机分成缺血再灌注组和硝酸甘油组 ,缺血再灌注组不给予任何药物 ,保持基础状态 ,单纯给与左冠状动脉前降支结扎 180 min,再灌注 12 0 min,在持续缺血和再灌注阶段行心肌声学造影 ,硝酸甘油组 ,用微量静脉泵以 2μg/(kg· min)速度静滴硝酸甘油 1h,2 4 h后结扎左冠状动脉前降支 ,其余步骤同缺血再灌注组。于左室乳头肌水平测定正常灌注区与缺血低灌注区心肌视频密度时间 -强度曲线参数 ,及缺血和再灌注阶段左室壁造影剂显影缺损区 (分别代表心肌危险区面积和坏死区面积 ) ,并与伊文思蓝及红四氮唑 (triphenyl tetrazolium chloride,TTC)心肌组织染色结果对照。结果　心肌造影时间 -强度曲线中 ,两组缺血低灌注区峰值强度 ,时间 -强度曲线下面积 ,比正常灌注区明显减低 ,峰值减半时间比正常灌注区延长 ,差异有显著性 ,缺血再灌注组、缺血低灌注区与正常灌注区心肌视频密度时间 -强度曲线参数比值较硝酸甘油组降低更明显 ,差异有显著性 ,MCE所测定的心肌坏死区面积与危险区面积之比与伊文思蓝及 TTC心肌组织染色结果成正相关。硝酸甘油可使心肌     

实时心肌超声造影定量评价犬急性心肌梗死缺血心肌的实验研究

目的探讨实时心肌超声造影(RT-MCE)技术定量评价静息状态下急性心肌梗死犬缺血心肌血流量(MBF)的应用价值。方法18只健康开胸犬均结扎冠状动脉前降支3h建立急性前壁心肌梗死模型。分别于结扎前和结扎3h后经股静脉匀速推注造影剂(C3F8)行RT-MCE检查,并采集动态心尖四腔、二腔和左室长轴观图像待分析。处死犬游离心脏后,行伊文思蓝(Evansblue)和三苯基氯化四氮唑(TTC)双染色。在MCE时间-强度曲线上测量A值(平台期峰值强度)和β值(曲线斜率),计算正常心肌和缺血心肌的血流量(MBF)。结果18只犬均成功建立急性前壁心肌梗死模型。冠状动脉前降支结扎前,RT-MCE显示18只犬心肌灌注良好;结扎3h后,MCE显示受累节段心肌出现灌注减少和灌注缺损。与病理染色结果对照:肉眼观察MCE定性诊断缺血心肌的敏感性为81.8%、特异性为87.4%;诊断梗死心肌的敏感性为60.0%、特异性为89.1%;静息状态下,以MBF<6.81ml.min-1.g-1诊断缺血心肌的敏感性为100%、特异性为77.1%,受试者特征工作曲线(ROC)下面积为0.977。结论RT-MCE技术定量诊断缺血心肌优于定性诊断,MBF<6.81ml.min-1.g-1可作为判断静息状态下犬急性心肌缺血的参考阈值。     

Identification of residual ischemia,infarction, and microvascular impairment in revascularized myocardial infarction using 64‐slice MDCT

This study aimed to assess the potential of 64‐slice MDCT in characterizing revascularized infarcted myocardium at the cellular and microvascular levels. Pigs (n = 7) underwent 2 h left anterior descending coronary artery occlusion/reperfusion. In acute (2–4 h) and subacute (1 week) infarction, first‐pass perfusion (FPP) (1 ml/kg of 300 mg/ml Omnipaque) was performed using a cine (rotation time 60 s/bpm) non‐ECG gated sequence (mAS/kV = 100/120). Delayed contrast enhanced images (DE) (mAS/kV = 650/120) were acquired every 2 min for 10 min to determine the kinetics of Omnipaque and to define infarcted myocardium and microvascular impairment (representing microvascular obstruction and/or no‐ or low‐reflow phenomenon). Maximum upslope, maximum attenuation and time to the peak were measured from FPP plots. 2,3,5‐Triphenyltetrazolium‐chloride (TTC) was used to define true infarction in the excised hearts. Hyperenhanced myocardium on DE was measured and compared with TTC. The contrast media caused minor beam hardening and X‐ray scatter on FPP. The above‐mentioned perfusion parameters significantly differed between remote and acute infarction. Infarcted myocardium showed two patterns of enhancement on DE, hyperenhanced rim representing the perfused infarction and hypoenhanced core representing a microvascular impaired region, with significantly different attenuation. The extent of infarction on DE‐MDCT decreased over the course of 1 week and did not differ from TTC. Post‐processed FPP semi‐quantitative images showed a decline in myocardial blood volume and flow in acute revascularized infarction. In conclusion, modern MDCT has the potential to identify residual ischemia on FPP and microvascular impairment and infarction on DE images. Copyright © 2008 John Wiley & Sons, Ltd.     

Real-Time Myocardial Contrast Echocardiography in Rat: Infusion Versus Bolus Administration

To compare the feasibility of real-time myocardial contrast echocardiography (MCE) in rats with infusion and bolus administration of a second-generation ultrasound contrast agent BR1. B-mode real-time MCE was performed in 12 Sprague Dawley rats following the BR1 infusion or bolus injection. The myocardium signal intensity (SI) was plotted against time and was fitted to exponential functions. The plateau SI (A) and rate of SI increase (β) for the infusion study and peak signal intensity (PSI) for the bolus study were obtained. ^99mTc-Sestamibi and Evans blue were used to assess myocardial blood perfusion and to calculate the myocardium perfusion defect area ex vivo. High-quality real-time MCE images were successfully obtained using each method. At baseline, all LV segments showed even contrast distribution. Following left anterior descending coronary artery (LAD) ligation, significant perfusion defect was observed in LAD beds with a significantly decreased A* β and PSI values compared with LCx beds (Infusion: A*β _LAD: 5.42 ± 1.57dB, A*β _LCx: 46.52 ± 5.32dB, p < 0.05; Bolus: PSI _LAD: 2.11 ± 0.67dB, PSI _LCx: 20.68 ± 0.72 dB, p < 0.05), which was consistent with ^99mTc-Sestamibi distribution findings. Myocardial perfusion defect areas, assessed by both methods, showed no differences and showed good correlation with Evans blue staining. ED frames were more favorable for imaging analysis. Both infusion and bolus administration of the contrast agent combined with real-time MCE technique can provide a reliable and noninvasive approach for myocardial perfusion assessment in rats and the infusion method was more suitable for quantitative analysis of myocardial blood flow. (E-mail: suhaili@fmmu.edu.cn)     

急性心肌梗塞后危险区与梗塞区的识别

目的　探讨急性心肌缺血损伤后危险区与梗塞区的识别方法。方法　成年健康家兔 8只分别制作阻塞性心肌梗塞和缺血再灌注心肌梗塞模型 ,伊文思蓝和TTC染色分别确定缺血区和梗塞区 ,染色前行MRI检查 ,放射微球 (99mTc MAA)测量心肌血流量作为标准对照 ,光镜和电镜检查验证染色结果。结果　伊文思蓝染色正常心肌呈蓝色 ,危险心肌和梗塞心肌染色阴性 ,TTC染色正常心肌和危险心肌呈砖红色 ,梗塞心肌染色阴性 ,染色确定的病变部位与MRI完全一致。危险和梗塞心肌血流量较正常心肌显著减少 ,病理损伤程度较正常心肌明显严重。结论　伊文思蓝和TTC染色是动物实验中确定危险与梗塞心肌的可靠方法。     

Multidetector-row computed tomographic evaluation of myocardial perfusion in reperfused chronic myocardial infarction: value of color-coded perfusion map in a porcine model

We aimed to develop color-coded CT perfusion maps (CPM) of infarcted myocardium and assess the utility of CPM in evaluating ischemic heart disease on a cardiac multi-detector CT (MDCT) in a porcine reperfused-myocardial-infarction model. Myocardial infarctions were induced by 30 min occlusions of the proximal left anterior descending coronary artery (LAD) in 17 healthy adult female pigs. First-pass and 5 min-delayed cardiac MDCTs were performed after 4 weeks of LAD occlusion. Myocardial CPMs were obtained by using the CPM program. Triphenyltetrazolium chloride (TTC)-staining was performed on the cardiac specimens. We analyzed the intermodality agreement on the size and location of the myocardial infarctions. TTC staining revealed myocardial infarction in 16 of 17 pigs, and 15 of these (94%) showed matched infarcts on the CPM and first-pass images. The areas of perfusion deficit noted in early arterial phase images and CPM coincided exactly with the areas of poor TTC staining in 12 of 15 pigs (80%). In the three remaining pigs, the areas of poor TTC staining were larger than those of a perfusion deficit demonstrated by either early arterial phase images or CPM. The agreement between these tests is calculated to be moderate to good (k = 0.736, P < 0.05). Ten myocardial segments in 4 of the 15 pigs (27%) with hypoattenuated myocardium showed a delayed enhancement on the 5 min-delayed images. Contrast-enhanced MDCT was useful and accurate in detecting chronic myocardial infarction; CPM was helpful in visualizing the infarcted myocardium.     

经静脉声学造影实时三维超声心动图测量左室心肌重量的实验研究

目的探讨经静脉声学造影实时三维超声心动图(RT-3DE)测量左室心肌重量的具体方法及其准确性. 方法氟碳气体造影前后采用RT-3DE对13条实验犬心脏进行探查.根据心尖长轴八平面法勾画左室心肌体积,再和心肌密度相乘计算左室重量.并与犬离体左室称重结果进行对比分析. 结果造影前后RT-3DE左室心肌重量计算结果分别为(57.51±11.42)g和(54.63±9.62)g,均与犬离体心脏左室心肌实际称重结果(55.62±9.34)g明显相关,但造影后RT-3DE的相关性更好(r=0.99 vs r=0.95).结论声学造影RT-3DE可显著提高左室心肌重量测量的准确性.     

Myocardial perfusion and wall motion in infarction border zone: assessment by myocardial contrast echocardiography.

Several mechanisms have been proposed to explain the decreased wall motion (WM) at the borders of myocardial infarction (MI). We used myocardial contrast echocardiography (MCE) to investigate the relation of perfusion to WM in infarcted border zones (BZs) 6 weeks after MI in 5 sheep. After quantifying the extent of WM abnormality and the perfusion defect, normal (NL), infarcted, and BZs were defined. Peak intensity after contrast was measured in acoustic units (AU). Radiolabeled microspheres were injected to measure regional blood flow. The heart was stained with 2,3, 5-triphenyltetrazolium chloride (TTC). The perfusion defect on MCE was 33% +/- 7% of the total myocardial area and correlated well with TTC (r = 0.92, P <.03). The BZ was 8% +/- 5% of the total myocardial area. Peak intensity after contrast was decreased in MI compared with BZ and NL (MI: 2.5 +/- 1.9 AU, BZ: 8.0 +/- 3.8 AU, P <.005; NL: 10.2 +/- 6.9 AU, P <.02) and comparable in NL and BZ. The blood flow measured by microspheres was not different in NL and BZ but was decreased in MI (NL: 1.6 mL/g/min, BZ: 1.5 +/- 0.5 mL/g/min, MI: 0.7 +/- 0.5 mL/g/min; P <.0001). In this model of chronic ovine MI, the BZ was small and its perfusion was preserved. These findings support the hypothesis that tethering of normal myocardial segments explains the abnormal wall motion noted at the borders of MI.     

Feasibility of dynamic CT-based adenosine stress myocardial perfusion imaging to detect and differentiate ischemic and infarcted myocardium in an large experimental porcine animal model

The purpose of the study is feasibility of dynamic CT perfusion imaging to detect and differentiate ischemic and infarcted myocardium in a large porcine model. 12 Country pigs completed either implantation of a 75 % luminal coronary stenosis in the left anterior descending coronary artery simulating ischemia or balloon-occlusion inducing infarction. Dynamic CT-perfusion imaging (100 kV, 300 mAs), fluorescent microspheres, and histopathology were performed in all models. CT based myocardial blood flow (MBF_CT), blood volume (MBV_CT) and transit constant (K_trans), as well as microsphere’s based myocardial blood flow (MBF_Mic) were derived for each myocardial segment. According to histopathology or microsphere measurements, 20 myocardial segments were classified as infarcted and 23 were ischemic (12 and 14 %, respectively). Across all perfusion states, MBF_CT strongly predicted MBF_Mic (β 0.88 ± 0.12, p < 0.0001). MBF_CT, MBV_CT, and K_trans were significantly lower in ischemic/infarcted when compared to reference myocardium (all p < 0.01). Relative differences of all CT parameters between affected and non-affected myocardium were higher for infarcted when compared to ischemic segments under rest (48.4 vs. 22.6 % and 46.1 vs. 22.9 % for MBF_CT, MBV_CT, respectively). Under stress, MBF_CT was significantly lower in infarcted than in ischemic myocardium (67.8 ± 26 vs. 88.2 ± 22 ml/100 ml/min, p = 0.002). In a large animal model, CT-derived parameters of myocardial perfusion may enable detection and differentiation of ischemic and infarcted myocardium.     

速度向量成像联合小剂量多巴酚丁胺负荷实验评价兔心肌梗死后存活心肌

目的 评价速度向量成像(VVI)联合小剂量多巴酚丁胺负荷实验检测兔心肌梗死模型存活心肌的价值。方法 结扎新西兰大白兔冠状动脉左心室支,建立心肌梗死兔模型。于术后8周对实验动物行小剂量多巴酚丁胺负荷实验,采用VVI检测局部室壁给药前后应变及应变率的改变;处死实验动物后,取心脏进行氯化三苯四氮唑(TTC)染色观察坏死心肌,以TTC结果为金标准,计算VVI诊断存活心肌的敏感度和特异度。结果 给予小剂量多巴酚丁胺后,非存活心肌节段应变和应变率较给药前均无明显改变(P均>0.05);存活节段收缩期应变和应变率随剂量增加而增加,与给药前比较差异均有统计学意义(P均<0.05),舒张期应变率亦有增加趋势,与给药前比较差异无统计学意义(P>0.05)。VVI联合小剂量多巴酚丁胺负荷实验诊断存活心肌的敏感度和特异度在左心室长轴切面为77.42%(24/31)和82.35%(42/51),在左心室短轴切面为84.31%(43/51)和88.73%(126/142)。结论 VVI联合小剂量多巴酚丁胺负荷实验评价心肌梗死后存活心肌准确、无创,具有潜在临床应用价值。     

SonoVue微泡介导转染Ang-1基因治疗急性心肌梗死

目的 探讨SonoVue微泡介导转染血管生成素-1(Ang-1)基因治疗急性心肌梗死的可行性.方法 27只中国家兔结扎冠状动脉左回旋支制成急性心肌梗死模型后随机分为4组:第1组(n=7,注射微泡+Ang-1+超声照射组)、第2组(n=7,单纯注射微泡+超声照射组)、第3组(n=7,单纯注射Ang-1+超声照射组)、第4组(n=6,空白对照组),于基因转染前后分别行常规超声心动图检查及心肌声学造影,并于处死后取心肌组织行RT-PCR检测Ang-1 mRNA表达.结果 第1组基因转染后2周常规超声心动图示左室射血分数(LVEF)显著提高(P<0.01),心功能改善,心肌声学造影可见术后充盈缺损处出现片状造影剂回声,RT-PCR可检测出Ang-1 mRNA表达,余各组则无明显心功能改善及造影剂充填,RT-PCR亦无法检测出Ang-1表达.结论 超声微泡可介导Ang-1基因成功转染至缺血心肌,改善缺血心肌微循环及心功能,对急性心肌梗死具有治疗作用.