缺血心肌梗死模型大鼠中等强度运动后梗死面积的变化

背景:目前对心肌梗死的急性期是否能进行适量的运动,且适量的运动是否对梗死心肌修复与再生有积极的意义,尚存在很大的争议。目的:观察中等强度运动对心肌梗死大鼠梗死面积的影响。方法:将48只SD大鼠随机分为雌、雄训练组和雌、雄对照组,每组12只。结扎大鼠左冠状动脉前降支建立左心室前壁梗死模型。造模24h,训练组大鼠进行30min/d的跑台训练,强度为20m/min,0%grade,共持续12d;对照组造模后正常饲养。2周后,对大鼠心肌行常规Masson’sTrichrome染色,观察梗死面积和左心室几何参数的变化。结果与讨论:造模2周,训练组和对照组大鼠的死亡率十分接近(22%vs.20%)。训练组(雌、雄)的心肌梗死面积明显小于对照组(P<0.05),梗死边缘区室壁厚度大于对照组(P<0.05),梗死区室壁最小厚度也大于对照组,但差异无显著性意义(P>0.05)。说明心肌梗死急性期即进行中等强度的跑台训练不但没有明显降低大鼠的存活率,还能有效减小缺血心肌的梗死面积、改善左心室重构,且上述作用没有性别差异。     

宽高频超声对大鼠心肌梗死模型左心室形态结构变化的分型研究

目的探讨不同病理分型大鼠心肌梗死模型左心室形态结构变化的超声表现。方法对48只SD大鼠实施开胸手术,其中41例结扎左冠状动脉前降支(LAD)(实验组),7例假手术组仅打开心包膜。术后4周采用10~22MHz的宽高频超声测定左心室形态、结构和功能,并与病理结果进行比较分析。结果按照心肌梗死的轻、中、重度病理分类,不同梗死程度的左心室形态在二维超声显像中表现为短轴和长轴的不同变化;心肌梗死大鼠左心室内腔和肌壁的几何形态失真,表现为梗死部位即瘢痕组织部位肌壁薄、回声增强且不均匀;斑痕组织的部位、大小与病变程度相关,并与病理改变相一致。轻、中、重度心肌梗死模型心肌前壁均变薄,中度涉及侧壁,重度后壁亦有改变。随着心肌梗死程度的加重,左心室缩短分数逐渐下降。结论经胸宽高频超声心动图可以在大鼠心脏的短轴和长轴切面直接显示心肌梗死发生的部位、范围和程度,准确评价大鼠左心室形态结构和功能变化。     

缺血心肌梗死模型大鼠中等强度运动后梗死面积的变化

背景：目前对心肌梗死的急性期是否能进行适量的运动,且适量的运动是否对梗死心肌修复与再生有积极的意义,尚存在很大的争议。目的：观察中等强度运动对心肌梗死大鼠梗死面积的影响。方法：将48只SD大鼠随机分为雌、雄训练组和雌、雄对照组,每组12只。结扎大鼠左冠状动脉前降支建立左心室前壁梗死模型。造模24h,训练组大鼠进行30min/d的跑台训练,强度为20m/min,0%grade,共持续12d;对照组造模后正常饲养。2周后,对大鼠心肌行常规Masson’sTrichrome染色,观察梗死面积和左心室几何参数的变化。结果与讨论：造模2周,训练组和对照组大鼠的死亡率十分接近（22%vs.20%）。训练组（雌、雄）的心肌梗死面积明显小于对照组（P〈0.05）,梗死边缘区室壁厚度大于对照组（P〈0.05）,梗死区室壁最小厚度也大于对照组,但差异无显著性意义（P〉0.05）。说明心肌梗死急性期即进行中等强度的跑台训练不但没有明显降低大鼠的存活率,还能有效减小缺血心肌的梗死面积、改善左心室重构,且上述作用没有性别差异。     

Echocardiographic evaluation of ventricular remodeling in a mouse model of myocardial infarction.

Gene-targeting in mice is a powerful tool to define molecular mechanisms of ischemic heart disease that determine infarct size, postinfarct left ventricular (LV) remodeling, and arrhythmogenesis. Coronary ligation in mice is becoming a widely used model of myocardial infarction (MI), but the pathophysiologic consequences of MI in mice and its relevance to human MI have not been fully elucidated. To characterize structural and functional changes during evolving MI, we analyzed 2-dimensional-based reconstruction of the left ventricle by noninvasive echocardiography obtained 1 day and 1 week after surgical ligation of the left anterior descending coronary artery in mice. Sequential 2-dimensional short-axis cineloops of the left ventricle were used to measure LV mass, and LV volumes at end-diastole and end-systole. Echocardiographic infarct size was estimated by measuring the volume of akinetic LV segments. Histologic infarct size was measured by planimetry of 9 transverse sections of each heart. There was close correlation between the 2 methods (31% +/- 20% of LV mass and 34% +/- 17% of LV area, respectively; y =.83x + 7.9, r = 0.96, P <.01). LV volumes at end diastole increased significantly between 1 day and 1 week (51 +/- 17 microL vs 78 +/- 46 microL, respectively, P <.05). The relative change in LV volumes at end diastole varied as a function of infarct size (r = 0.93, P <.01). LV mass and the extent of hypertrophy of noninfarcted segments also varied with infarct size (r = 0.92, P <.01; r = 0.90, P <.01, respectively). Thus, echocardiography is an accurate noninvasive tool for determination of infarct size and quantitative characterization of postinfarct remodeling in the mouse model of MI. Alterations in cardiac structure and function after coronary ligation in mice closely resemble pathophysiologic changes in human ischemic heart disease.     

Semaphorin 3A attenuates electrical remodeling at infarct border zones in rats after myocardial infarction

Electrical remodeling at infarct border zone has been shown to contribute to the occurrence of ventricular arrhythmias after myocardial infarction (MI). Electrical remodeling is causally associated with sympathetic neural remodeling in MI. Semaphorin 3A (Sema3A), a potent neural chemorepellent for sympathetic axons, has been demonstrated to suppress sympathetic neural remodeling after MI. In the present study, we investigated whether treatment with Sema3A can ameliorate electrical remodeling at infarct border zones using a rat model of MI. Wistar rats underwent sham operation (n = 20), the ligation of left coronary artery (MI group, n = 30), MI with control adenovirus (Ad group, n = 30), and MI with Sema3A adenovirus (Sema3A group, n = 30). Eight weeks after treatment, electrophysiological properties including heart rate variability (HRV), monophasic action potential duration (MAPD) and effective refractory period (ERP) and the expression of arrhythmia-related ion channel proteins including Kv4.2, KChIP2 and Kir2.1 at the infarcted border of the left ventricle were examined. These channel proteins may be required for maintaining normal heart rhythm. Compared with the Ad group, Sema3A significantly increased HRV and shortened MAPD and ERP (all p < 0.05). The expression levels of Kv4.2, KChIP2 and Kir2.1 proteins were significantly decreased in MI group and Ad group, compared to sham control. In contrast, the expression levels of these proteins were restored in Sema3A group, which may represent the molecular basis of the Sema3A-mediated inhibition of electrical remodeling. In conclusion, Sema3A can ameliorate electrical remodeling at infarct border zones after MI.     

Assessment of infarct size and myocardial function in mice using transesophageal echocardiography.

BACKGROUND: Because transthoracic echocardiography (TTE) has significant limitations in assessing changes consequent to myocardial infarction (MI) in mice, we studied two novel methods to characterize such infarcts. METHODS: Large MIs were produced by proximal left coronary artery ligation, and small MIs by distal left coronary artery ligation. Serum cardiac troponin I levels were measured 24 hours postoperatively. At 2 weeks, mice underwent transesophageal echocardiography (TEE) and TTE. Infarct sizes were determined histologically. RESULTS: Surviving mice were classified according to infarct size. TEE identified all histologically proven large infarcts, and 4 of 5 small infarcts. TTE identified 4 of 5 large infarcts, but only 1 of 5 small infarcts. TEE-derived fractional area change, but not TTE-estimated left ventricular fractional shortening, was significantly different among large, small, and sham infarcts. Cardiac troponin I showed excellent correlation with infarct size and mortality. CONCLUSIONS: Cardiac troponin I was found to predict infarct size and mortality, whereas TEE proved superior to TTE in determining infarct size and/or myocardial function in a murine MI model. These tools should provide more accurate assessments in preclinical studies of ischemic cardiomyopathy.     

hVEGF165腺相关病毒对心肌梗死大鼠心功能的影响

目的探讨直接心肌注射基因重组hVEGF165腺相关病毒（rAAV—hVEGF165）对急性心肌梗死大鼠心功能的影响。方法取81只雄性Sprague—Dawley大鼠,制备急性,0．／肌梗死大鼠模型。将心肌梗死大鼠模型随机分成4组：假手术组15只;心肌梗死组25只;生理盐水纽25只;VEGF组16只。生理盐水组和VEGF组分别接受生理盐水或rAAV—hVEGF165100μ1分3点注射于梗死交界处心肌内。于注射4周后测定心肌组织VEGF含量、超声心动图参数、梗死范围、微血管数量、心钠素（atrial natriuretic peptide,ANP）水平。结果假手术组中3只大鼠、心肌梗死组中13只大鼠、生理盐水组中15只大鼠、VEGF组中7只大鼠死亡,43只大鼠进入研究。VEGF组心肌梗死范围较心肌梗死组和生理盐水组明显减小（38．6±3．0）％VS（42．5±3．8）％、（42．5±2．6）％（P〈0．05）。VEGF组的左心室射血分数显著高于心肌梗死组和生理盐水组（61．11±8．37）％VS（44．17±5．31）％、（39．40±5．48）（P〈0．01）。VEGF纽心肌组织中VEGF含量较心肌梗死组和生理盐水组有所增加。血管计数显示,VEGF组有更多的新生血管形成（522．38±82．14）mm2vs（419．99±32．17）mm2、（420．86±16．50）mm2（P〈0．01）。结论梗死区交界处心肌内直接注射rAAV-hVEGF165能够显著改善急性心肌梗死大鼠的心功能,缩小梗死范围,促进心肌内新生血管的形成。     

Effect of transplantation of bone marrow stem cells on myocardial infarction size in a rabbit model

BACKGROUND:

Intravenous transplantation has been regarded as a most safe method in stem cell therapies. There is evidence showing the homing of bone marrow stem cells (BMSCs) into the injured sites, and thus these cells can be used in the treatment of acute myocardial infarction (MI). This study aimed to investigate the effect of intravenous and epicardial transplantion of BMSCs on myocardial infarction size in a rabbit model.

METHODS:

A total of 60 New Zealand rabbits were randomly divided into three groups: control group, epicardium group (group I) and ear vein group (group II). The BMSCs were collected from the tibial plateau in group I and group II, cultured and labeled. In the three groups, rabbits underwent thoracotomy and ligation of the middle left anterior descending artery. The elevation of ST segment >0.2 mV lasting for 30 minutes on the lead II and III of electrocardiogram suggested successful introduction of myocardial infarction. Two weeks after myocardial infarction, rabbits in group I were treated with autogenous BMSCs at the infarct region and those in group II received intravenous transplantation of BMSCs. In the control group, rabbits were treated with PBS following thoracotomy. Four weeks after myocardial infarction, the heart was collected from all rabbits and the infarct size was calculated. The heart was cut into sections followed by HE staining and calculation of infarct size with an image system.

RESULTS:

In groups I and II, the infarct size was significantly reduced after transplantation with BMSCs when compared with the control group (P<0.05). However, there was no significant difference in the infarct size between groups I and II (P>0.05).

CONCLUSION:

Transplantation of BMSCs has therapeutic effect on MI. Moreover, epicardial and intravenous transplantation of BMSCs has comparable therapeutic efficacy on myocardial infarction.KEY WORDS: Bone marrow stem cells, Acute myocardial infarction, Epicardial transplantation, Intravenous transplantation, Infarct size, Rabbit     

High‐Resolution Optical Mapping of Ventricular Tachycardia in Rats with Chronic Myocardial Infarction

Background: Ventricular tachycardia (VT) is a common cause of mortality in post‐myocardial infarction (MI) patients, even in the current era of coronary revascularization treatment. We report a reproducible VT model in rats with chronic MI induced by ischemia‐reperfusion and describe its electrophysiological characteristics using high‐resolution optical mapping. Methods: An MI was generated by left anterior descending coronary ligation (25 minutes) followed by reperfusion in 20 rats. Electrophysiology study and optical mapping were performed 5 weeks later using a Langendorff‐perfused preparation and compared to normal rats. Results: The conduction velocity of the MI border zone was decreased to 53% of the normal areas remote from the infarct (0.37 ± 0.16 m/sec vs 0.70 ± 0.09 m/sec, P < 0.0001). The rate of VT inducibility in MI rats was significantly greater than in normal control rats (70% vs 0%, P = 0.00002). VT circuits involving the infarct area were identified with optical mapping in 83% MI rats. In addition, fixed and functional conduction block were observed in the infarct border zone. Conclusion: This ischemia‐reperfusion MI rat model is a reliable VT model, which simulates clinical revascularization treatment. High‐resolution optical mapping in this model is useful to study the mechanism of VT and evaluate the effects of therapies. (PACE 2010; 33:687–695)     

Artemisinin attenuates post-infarct myocardial remodeling by down-regulating the NF-κB pathway

Myocardial infarction (MI) leads to progressive left ventricular (LV) dilatation and is associated with interstitial fibrosis in the non-infarcted myocardium. The NF-κB signaling pathway plays an important role in ventricular remodeling after MI. Recent studies have indicated that the anti-malarial agent artemisinin can inhibit NF-κB activation, which may attenuate post-infarct myocardial remodeling. In this study, we investigated the effect of artemisinin on post-infarct myocardial remodeling using a rat model of MI. Adult male Sprague Dawley rats were divided into a sham group (n = 10) and MI groups that were treated either with oral gavage of artemisinin (75 mg/kg/day, n = 20) or vehicle (0.5% carboxymethyl cellulose, n = 20) three times a day for 4 weeks. Each treatment was started at 24 hours after ligation of the left anterior descending coronary artery. Four weeks after MI, the artemisinin-treated group showed a significantly improved survival rate compared with that of the vehicle-treated group (65% vs. 40%, P < 0.05). Although infarct size was similar in both groups, echocardiography showed significant improvements in cardiac function and left ventricular dimensions in the artemisinin-treated group. Moreover, the degree of myocardial fibrosis and elevated levels of fibrosis-related factors [transforming growth factor-β1, collagen type I, matrix metalloproteinase (MMP)-2 and MMP-9] in the non-infarcted myocardium were remarkably ameliorated by artemisinin (all P < 0.05). Importantly, artemisinin inhibited the NF-κB pathway by blocking IKBα phosphorylation. In conclusion, artemisinin may attenuate post-infarct myocardial remodeling by down-regulating the NF-κB pathway.     

BM-573, a dual thromboxane synthase inhibitor and thromboxane receptor antagonist,prevents pig myocardial infarction induced by coronary thrombosis

The aim of this study was to characterize the effects of BM-573 [N-terbutyl-N'-[2-(4'-methylphenylamino)-5-nitro-benzenesulfonyl] urea], a novel dual thromboxane A2 receptor antagonist and thromboxane synthase inhibitor, on myocardial infarction induced by topical ferric chloride (FeCl3) application to the left anterior descending (LAD) coronary artery in anesthetized pigs. All control animals (n = 6) developed an occlusive thrombus in the LAD coronary artery. The mean infarct size, revealed by triphenyl tetrazolium chloride (TTC), and the area at risk, evidenced by Evans blue, corresponded to 35.3 +/- 2.2 and 36.9 +/- 2.1% of the left ventricular mass, respectively. In the BM-573-treated group (n = 6), a drug infusion (10 mg. kg-1. h-1) started 30 min before FeCl3 application and continued throughout the experimentation. Among the BM-573-treated group, four pigs did not develop coronary artery thrombus and their myocardium appeared healthy. Histopathological examination of FeCl3-injured coronary artery revealed an occlusive and adherent thrombus in control group, while pretreatment with BM-573 prevented thrombus formation. In infarcted zones, lack of desmin staining and muscle structure disorganization were obvious. Depletion of myocardial ATP content was observed in the myocardial necrotic region of the control group, but not in myocardial samples of BM-573-treated pigs that did not develop myocardial infarction. When BM-573 prevented LAD artery occlusion, the area under the curve of plasmatic troponin T was reduced by 77% over 6 h. These data suggest that BM-573 could be useful for the prevention of myocardial infarction.     

Ultrasound Bio-microscopy for Measurement of Coronary Artery Flow and Estimation of Infarct Size in a Mouse Model of Acute Myocardial Infarction

Ultrasound bio-microscopy was used to measure hemodynamic changes in the left main coronary artery after myocardial infarction (MI), and its usefulness in estimating infarct size was evaluated. MI was induced by left anterior descending artery ligation. Diastolic peak velocity (V_d), mean flow velocity (V_mean) and the velocity-time integral (VTI) were measured 2 and 6 h after MI. Serum troponin I levels were assayed 2, 6 and 12 h after MI. At 2 h, V_mean and VTI significantly differed between mice that underwent low and high left anterior descending artery ligation; V_d, V_mean and VTI were correlated with infarct size (r = −0.557, −0.693 and −0.672, respectively; all p < 0.01). Infarct size was more strongly correlated with 2-h ultrasound bio-microscopy measurements than with 2-h serum troponin I level. Measurement of coronary artery blood flow by ultrasound bio-microscopy may be useful for early estimation of infarct size in mice.     

Favorable left ventricular remodeling following large myocardial infarction by exercise training. Effect on ventricular morphology and gene expression.

Continued adverse remodeling of myocardium after infarction may lead to progressive ventricular dilation and heart failure. We tested the hypothesis that exercise training in a healed myocardial infarction-dysfunction rat model can favorably modify the adverse effects of ventricular remodeling including attenuation of abnormal myosin gene expression. Sprague-Dawley rats were subjected to either proximal LAD ligation or sham operation. At 5 wk after the operation, animals were randomly assigned to sedentary conditions or 6 wk of graduated swim training, creating four experimental groups: infarct sedentary (IS), infarct exercise (IE), sham sedentary (SS), and sham exercise (SE). At 11 wk all rats were sacrificed and analyzed. Compared to sedentary infarct controls, exercise training attenuated left ventricular (LV) dilation and allowed more hypertrophy of the non infarct wall. The exercise-trained hearts also showed a reduction in the estimated peak wall tension. Northern blot analysis showed an increase in beta-myosin heavy chain expression in the hearts of the sedentary infarction group soon after infarction when compared to sham controls. However, with exercise training, there was a significant attenuation of the beta-myosin heavy chain expression in the myocardium. Exercise training in a model of left ventricular dysfunction after healed myocardial infarction can improve the adverse remodeling process by attenuating ventricular dilation and reducing wall tension. The abnormal beta-myosin expression was also attenuated in the exercise trained group. This is evidence that abnormal gene expression following severe myocardial infarction dysfunction can be favorably modified by an intervention.     

Effects of anemia and blood transfusion in acute myocardial infarction in rats

BACKGROUND: The optimal hemoglobin (Hb) level in acute myocardial infarction (MI) is unknown. The goal of this study was to determine the optimal Hb concentration in acute MI and whether transfusion of fresh blood to correct anemia reduces myocardial injury and improves outcome.
STUDY DESIGN AND METHODS: Anemia was induced in rats by an iron-deficient diet and phlebotomy. MI was induced by left coronary artery ligation. Some rats received transfusion of fresh blood. Survival, hemodynamic measurements, and infarct size were determined 24 hours after MI.
RESULTS: Reduction of Hb to 80 to 90 and 70 to 80 g/L decreased 24-hour survival after MI to 42 and 47%, respectively (p < 0.05). Infarct size was increased in both 70 to 80 and 80 to 90 g/L anemic groups compared to the normal Hb group (p < 0.05). Cardiac function was decreased in anemic groups after MI (p < 0.01). Transfusion of fresh blood to increase Hb from 80 to 90 g/L to 100 g/L decreased infarct size (p < 0.05) and improved cardiac function (p < 0.05), and a trend toward better survival (73%) was observed. Transfusion from 80 to 90 g/L Hb to 120 g/L Hb was associated with larger infarct size (p < 0.05), decreased cardiac function (p < 0.05), and no improvement in survival (47%, p = NS).
CONCLUSION: Anemia increases infarct size and decreases cardiac function and survival in acute MI. Transfusion of anemic animals up to 100 g/L Hb with fresh blood reduces infarct size and improves cardiac function. However, transfusion to 120 g/L Hb did not demonstrate any additional benefit and was associated with larger infarcts.     

犬急性心肌梗死与再灌注的多层螺旋CT评价实验研究

目的探讨多层螺旋CT评价急性冠状动脉闭塞后心肌梗死及再灌注的能力.方法将12只杂种犬随机分成两组:①急性心肌梗死组(AMI),分别于结扎冠状动脉前、结扎后1 h和2 h进行CT平扫和增强扫描.②AMI再灌注组,分别于结扎前、结扎后1 h及再灌注30 min进行同样扫描.观察心肌梗死的病变部位及形态,测量每组正常心肌、心肌梗死部位在各个扫描时点的CT值,计算两者与左心室腔的CT值之比(M/L).结果12只犬结扎左前降支后1 h增强图像上左心室前壁或心尖区均有明显的低密度区形成.AMI组结扎后2 h图像缺血区的密度更为减低;AMI再灌注组再灌注30 min后病变的密度变化不明显.AMI组结扎后1 h与2 h的正常心肌与梗死心肌的CT值均值及两者与左心室腔的M/L均具有显著性差异(P＜0.001).AMI再灌注组结扎后1 h与再灌注后30 min正常心肌与梗死心肌的CT值均值及两者与左心室腔M/L也具有显著性差异(P＜0.001).结论急性冠脉闭塞后心肌梗死区MSCT表现为低密度,MSCT能够区分急性冠状动脉闭塞后梗死心肌与正常心肌.     

速度向量成像技术评价心肌梗死节段室壁径向收缩能力的价值

目的 探讨速度向量成像(VVI)技术评价心肌梗死节段径向收缩能力的价值.方法 将雄性Wister大鼠分为两组,一组结扎冠状动脉制成心肌梗死模型组(10只),另一组同样进行手术但不结扎冠状动脉作为对照组(14只).应用VVI技术对左室短轴乳头肌水平室壁径向应变及应变率进行分析.结果 心肌梗死组梗死节段(左室前壁及前间隔)径向应变及应变率较对照组相应节段明显减低,两组间差异具有统计学意义(P<0.05).对照组各节段室壁应变及应变率比较差异无统计学意义(P>0.05).结论 VVI技术能够定量评价心肌梗死节段室壁的径向收缩能力.     

不同时间经静脉移植人脐血单个核细胞对心肌梗死大鼠心功能及结构重构的影响

目的观察不同时间经静脉移植人脐血单个核细胞(HUCBC)对心肌梗死(MI)大鼠心功能及结构重构的影响。方法入选雄性Wistar大鼠共80只,结扎左前降支,制备心肌梗死模型,于梗塞后1d、5d、10d以及30d经尾静脉注入0.5ml人脐血[含单个核细胞(1～3)×107]或0.5ml磷酸盐缓冲溶液(PBS)。不使用免疫抑制剂。术后4周行超声心动图和血流动力学检查,随后处死大鼠,取出梗死心肌,以甲醛固定,进行苏木素伊红(HE)染色以及转移酶介导的三磷酸脱氧鸟苷-生物素刻痕末端标记(TUNEL)计算凋亡细胞。结果 PBS组大鼠左室明显扩大,梗死部位变薄。移植后瘢痕面积减少,室壁较对照组增厚。5d和10d移植瘢痕面积明显减小。与对照组相比,5d和10d移植大鼠左室射血分数(EF),左室压力最大变化率(±dp/dtmax)明显升高,左室收缩末内径(LVESD)明显减小,左室后壁(LVPW)增厚率更高。而梗死后10d移植EF,±dp/dtmax,以及LVPW增厚率的改善最明显。移植大鼠心肌和对照组相比凋亡细胞没有明显差异。结论大鼠心肌梗死后5d和10d经静脉移植HUCBC可以明显抑制心室重构,改善心功能。在梗死后第10天移植对梗死心肌的结构重塑改善最明显,但对细胞凋亡没有明显作用。     

微创开颅法局灶性大鼠脑梗死模型的实验研究

目的建立一种稳定的大鼠脑局灶性梗死模型，以用于脑梗死后神经干细胞移植的长期观察。方法37只大鼠随机分为实验组和对照组。微刨法经颞骨局部钻孔开颅，采用直接结扎大脑中动脉终段，同时永久结扎同侧颈总动脉、暂时性夹闭对侧颈总动脉的方法制备大鼠脑梗死模型。通过大鼠脑梗死后的神经功能评分、墨汁灌注、TTC染色、MRI成像结果对该模型进行评价。结果大鼠术后状态良好，实验组大鼠观察4周后死亡率低为6．25％。大鼠神经功能评分均为1分，墨汁灌注及TTC染色观察梗死范围局限于皮层，4周后MRI成像测量梗死体积稳定，平均为83．52mm^2。结论该模型对大鼠创伤小，梗死灶的位置和体积恒定，长期存活率高，为脑梗死后神经干细胞移植的研究提供了一种理想的动物模型。     

Acipimox-enhanced (18)F-fluorodeoxyglucose positron emission tomography for characterizing and predicting early remodeling in the rat infarct model

The rat myocardial infarction (MI) model is widely used to study left ventricular (LV) remodeling. In this study, acipimox-enhanced (18)F-Fluorodeoxyglucose (FDG) gated-positron emission tomography (PET) was assessed for characterizing and predicting early remodeling in the rat infarct model. Nineteen Wistar rats had surgical occlusion of the left anterior descending coronary artery and 7 were sham-operated. PET was scheduled 48 h and 2?weeks later for quantifying MI area and LV function. Segments with <50% of FDG uptake had histological evidence of MI (74?±?9% decrease in parietal thickness, fibrosis development). At 48 h, MI area was large (>35% of LV) in 6 rats, moderate (15-35% of LV) in 8 rats, limited (<15% of LV) in 5 rats and absent in the 7 sham rats. LV remodeling, assessed through the 2 weeks increase in end-diastolic volume, increased between rats with limited, moderate and large MI (+72?±?25, +109?±?56, +190?±?69 μl, respectively, P?=?0.007). This 3-groups classification allowed predicting 44% of the 2 weeks increase in end-diastolic volume, and additional 34% were predicted by heart rate at 48 h. The acipimox-enhanced FDG gated-PET technique provides efficient characterization and prediction of early remodeling in the rat infarct model.     

Wideband High‐Frequency Echocardiography to Evaluate Myocardial Infarct Size

Objective. This study was designed to validate the feasibility of wideband high‐frequency ultrasound imaging to resolve in vivo the degree, location, and morphologic changes of myocardial infarction (MI) in a rat model. Methods. The left anterior descending coronary artery was ligated in the test group (n = 41), and the sham control group did not have ligation (n = 7). The rats were examined with 10‐ to 22‐MHz echocardiography to evaluate the MI size, location, and geometric formation. Results. The endocardial chamber shape was deformed, with enlargement of the anteroposterior dimension and fractional shortening, and was comparable with the degree of MI both in short‐ and long‐axis sections of the left ventricle. Histologic analysis showed remodeling to different extents corresponding to different MI sizes (small, medium, and large). Conclusions. The results suggest that this technique can be used in vivo to evaluate the MI location, size, and morphologic changes corresponding to the extent of the injury.