Prior exercise training does not prevent acute cardiac alterations after myocardial infarction in female rats

OBJECTIVE:

This study aimed to investigate whether previous exercise training could prevent or attenuate acute cardiac alterations after myocardial infarction.

METHODS:

Female rats were submitted to swim training (1 h/day; 5 days/week) or allowed to remain sedentary for 8 weeks. Afterwards, they were randomly assigned to left coronary artery occlusion or sham surgery. After this procedure, the rats remained sedentary for one week until euthanasia. Cardiac structural and functional analyses were performed using Doppler echocardiography. The rats that had a moderate or large infarct size were included in the evaluations. The data (mean ± SEM) were analyzed using a two-way ANOVA model followed by Tukey''s post-hoc test.

RESULTS:

After the surgery, no significant difference between the exercise and sedentary groups was observed in the left ventricular infarct sizes (34.58±3.04 vs. 37.59±3.07). In another group of rats evaluated with Evans blue 1 h after myocardial infarction, no siginificant difference in the area at risk was observed between the exercised and sedentary rats (49.73±1.52 vs. 45.48±3.49). The changes in the left ventricular fractional areas for the exercised and sedentary myocardial infarction groups (36±2% and 39±3%, respectively) were smaller than those for the exercise sham surgery (ES, 67±1%) and sedentary sham surgery (SS, 69±2%) groups. The E/A was higher in the sedentary myocardial infarction (4.4±0.3) and exercised myocardial infarction (5.5±0.3) rats than in the SS (2.4±0.1) and ES (2.2±0.1) rats.

CONCLUSION:

Previous swim training of female rats does not attenuate systolic and diastolic function alterations after myocardial infarction induced by left coronary artery occlusion, suggesting that cardioprotection cannot be provided by exercise training in this experimental model.     

Short-term diabetes attenuates left ventricular dysfunction and mortality rates after myocardial infarction in rodents

OBJECTIVES:

To investigate the effects of hyperglycemia on left ventricular dysfunction, morphometry, myocardial infarction area, hemodynamic parameters, oxidative stress profile, and mortality rate in rats that had undergone seven days of myocardial infarction.

INTRODUCTION:

Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury.

METHODS:

Male Wistar rats were divided into four groups: control-sham, diabetes-sham, myocardial infarction, and diabetes + myocardial infarction. Myocardial infarction was induced 14 days after diabetes induction. Ventricular function and morphometry, as well as oxidative stress and hemodynamic parameters, were evaluated after seven days of myocardial infarction.

RESULTS:

The myocardial infarction area, which was similar in the infarcted groups at the initial evaluation, was reduced in the diabetes + myocardial infarction animals (23±3%) when compared with the myocardial infarction (42±7%, p<0.001) animals at the final evaluation. The ejection fraction (22%, p = 0.003), velocity of circumferential fiber shortening (30%, p = 0.001), and left ventricular isovolumetric relaxation time (26%, p = 0.002) were increased in the diabetes + myocardial infarction group compared with the myocardial infarction group. The diabetes-sham and diabetes + myocardial infarction groups displayed increased catalase concentrations compared to the control-sham and myocardial infarction groups (diabetes-sham: 32±3; diabetes + myocardial infarction: 35±0.7; control-sham: 12±2; myocardial infarction: 16±0.1 pmol min^-1 mg^-1 protein). The levels of thiobarbituric acid-reactive substances were reduced in the diabetes-sham rats compared to the control-sham rats. These positive adaptations were reflected in a reduced mortality rate in the diabetes + myocardial infarction animals (18.5%) compared with the myocardial infarction animals (40.7%, p = 0.001).

CONCLUSIONS:

These data suggest that short-term hyperglycemia initiates compensatory mechanisms, as demonstrated by increased catalase levels, which culminate in improvements in the ventricular response, infarcted area, and mortality rate in diabetic rats exposed to ischemic injury.     

短时高强度间歇运动训练心肌梗死模型大鼠心室重构及线粒体变化

BACKGROUND: It is unclear whether short-term high-intensity interval training (HIT) can be used to protect against myocardium injury after acute myocardial infarction, as well as the underlying mechanism.     

急性心肌梗死家兔心肌MtATPase表达和心肌细胞凋亡的变化

目的： 研究急性心肌梗死后线粒体能量代谢和心肌细胞凋亡的动态变化,探讨二者在缺血心肌细胞演变中的作用和意义。方法: 结扎家兔左冠状动脉主干建立实验性心肌梗死（AMI）模型,采用酶组织化学染色法和脱氧核苷转移酶介导的缺口末端标记技术检测梗死后0.5、1、2、4、8、12 h左室前壁线粒体腺苷三磷酸酶（MtATPase）和细胞凋亡的变化,结合显微图像分析技术定量测定酶活性平均积分吸光度值（IA）和凋亡指数（AI）。结果: (1)AMI 2 h,MtATPase表达开始下降,4 h显著减低,随着缺血时间延长,表达持续下降, 2、4、8、12 h IA分别为168.09±3.75、159.01±2.62、143.12±3.47和127.65±4.64,与对照组比较有明显差异（P<0.05）;(2)AMI 0.5 h仅见少数凋亡心肌细胞,随缺血时间延长,凋亡细胞数目显著增加,4 h达到高峰,然后开始下降,但12 h仍高于对照组, 0.5、1、2、4、8、12 h AI分别为4.74±0.75、10.96±1.06、17.28±1.75、26.83±2.06、20.41±1.52和8.91±0.74,与对照组比差异显著（P<0.01）。结论: 细胞凋亡是AMI心肌细胞一种重要的死亡形式,梗死心肌细胞的演变和线粒体能量代谢密切相关。     

左西孟旦对大鼠急性心肌梗死后心肌纤维化及心功能的影响

目的 探讨左西孟旦对心肌梗死（myocardial infarction,MI）大鼠心肌纤维化的影响及其作用机制。 方法 通过结扎大鼠左冠状动脉前降支建立MI模型。30只存活的MI大鼠随机分为模型组和左西孟旦组（Levo组）,每组15只。假手术组（n=10）的大鼠接受相同的外科手术,只是不进行动脉结扎。Levo组胃灌注左西孟旦4.67 μg·kg-1·d-1治疗28 d。假手术组和模型组大鼠同时给等量蒸馏水。采用二维超声心动图评价心功能,Masson-trichrome评价心肌纤维化程度,RT-qPCR检测COL1A1、COL3A1基因表达,Western blot检测SIRT1/TGF-β1/Smad3信号通路蛋白表达。 结果 超声心动图测量显示,与模型组相比,Levo组大鼠的左室收缩末期内径降低（P<0.05）,而射血分数和缩短分数显著升高（P<0.01）。Masson-trichrome显示,左西孟旦治疗可显著减少坏死心肌组织、抑制炎性细胞的浸润并减少胶原蛋白沉积。RT-qPCR分析显示,左西孟旦治疗显著降低了MI大鼠心肌组织中Ⅰ型和Ⅲ型胶原的含量（P<0.01）。Western blot检测显示,左西孟旦治疗可显著上调MI大鼠心肌组织中SIRT1蛋白表达（P<0.01）,下调TGF-β1和p-Smad3蛋白表达（P<0.01）。 结论 左西孟旦具有抗纤维化和心保护作用。这些作用可能通过SIRT1/TGF-β1/Smad3信号通路介导。     

心肌干细胞移植可短期内改善心肌梗死心电生理稳定性和提高室颤阈值

背景：课题组前期研究已证实心肌干细胞移植中期(6周)能有效改善心肌梗死大鼠的心电生理稳定性和室颤阈值。目的：比较心肌干细胞和骨髓间充质干细胞移植对心肌梗死大鼠心电生理学稳定性和室颤阈值的短期疗效差异。方法：取30只健康雄性SD大鼠,开胸结扎大鼠的左前降支冠状动脉建立心肌梗死动物实验模型,随机分成3组,分别为心肌干细胞移植组,骨髓间充质干细胞移植组,PBS对照组,每组10只。分别于建模成功2周后在梗死区心肌内局部注射0.1 mL PBS悬浮的5×10⁶ PKH26标记的心肌干细胞、0.1 mL PBS悬浮的5×10⁶ PKH26标记的骨髓间充质干细胞及0.1 mL PBS。植入2周后,再次开胸检测大鼠心脏梗死区、梗死边缘区、非梗死区的心电生理特性和室颤阈值。实验结束后,分离心脏梗死边缘区进行病理切片及荧光显微镜检查PHK26标记的心肌干细胞和骨髓间充质干细胞缝隙连接蛋白43表达情况。结果与结论：心肌干细胞移植组单极电图纠正的激动恢复时间离散度、电刺激所激发的恶性心律失常及梗死区、梗死边缘区、非梗死区的室颤阈值与PBS组、骨髓间充质干细胞移植组相比差异有显著性意义(P < 0.05);骨髓间充质干细胞移植组单极电图纠正的激动恢复时间离散度及非梗死区的室颤阈值与PBS组相比差异有显著性意义。病理结果提示在心肌干细胞组、骨髓间充质干细胞组梗死边缘区发现有心肌干细胞、骨髓间充质干细胞的存在。通过组织免疫荧光检测,PKH26标记的心肌干细胞表达较多的缝隙连接蛋白43,而PKH26标记的骨髓间充质干细胞很少表达缝隙连接蛋白43,PBS组不表达缝隙连接蛋白43。上述结果提示心肌干细胞移植短期内心电生理学特性改善的效应较骨髓间充质干细胞优越,且改善效应与缝隙连接蛋白43相关。 中国组织工程研究杂志出版内容重点：干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程     

Prognostic value of left atrium remodeling after primary percutaneous coronary intervention in patients with ST elevation acute myocardial infarction

The purpose of this study is to assess the relationship between left atrial (LA) size and outcome after acute myocardial infarction (AMI) in patients undergoing primary percutaneous coronary intervention (PCI) and to evaluate dynamic changes in LA size during long-term follow-up. Echocardiographic analyses were performed on 253 AMI patients (174 male and 79 female, 65.4 ± 13.7 yr) undergoing PCI. These subjects were studied at baseline and at 12 months. Clinical follow-up were done at 30.8 ± 7.5 months. We assessed LA volume index (LAVI) at AMI-onset and at 12-month. Change of LAVI was an independent predictor of new onset of atrial fibrillation or hospitalization for heart failure (P = 0.002). Subjects who survived the 12-month period displayed an increased LAVI mean of 1.86 ± 4.01 mL/m(2) (from 26.1 ± 8.6 to 28.0 ± 10.1 mL/m(2), P < 0.001). The subject group that displayed an increased LAVI correlated with a low left ventricular ejection fraction, large left ventricle systolic and diastolic dimensions and an enlarged LA size. In conclusion, change of LAVI is useful parameter to predict subsequent adverse cardiac event in AMI patients. Post-AMI echocardiographic evaluation of LAVI provides important prognostic information that is significantly greater than that obtained from clinical and laboratory parameters alone.     

糖原合成酶激酶3β过表达心肌干细胞移植治疗心肌梗死

BACKGROUND:The mechanism and effect of glycogen synthase kinase 3β (GSK-3β) in the differentiation of cardiac stem cells into cardiomyocytes are still unclear, although GSK-3β is closely related to the life activities of cells. OBJECTIVE:To investigate the changes of GSK-3β expression in the treatment of myocardial infarction in rats undergoing cardiac stem cell transplantation. METHODS:The isolation and culture of cardiac stem cells were performed in 10 neonatal rats. Lentivirus overexpressing GSK-3β or LacZ (control) was constructed and transferred into cardiac stem cells. Animal model of myocardial infarction was made in 30 Sprague-Dawley rats. Six weeks after model preparation, rat models were assigned into GSK-3β, LacZ or PBS group. GSK-3β or LacZ overexpressing cardiac stem cell solution or PBS in equal volume was injected into the rat myocardium, respectively. Four weeks after transplantation, the cardiac function and myocardial collagen production in rats were detected and compared. RESULTS AND CONCLUSION:Compared with the other two groups, the left ventricular ejection fraction was significantly higher, and the left ventricular end diastolic diameter was significantly lower in the GSK-3β group (P < 0.05). Hydroxyproline content, type I collagen mRNA, and type III collagen mRNA expression were significantly lower in the GSK-3β group than the other two groups (P < 0.05). Findings from Masson staining showed that the content of blue-stained collagen was significantly lower in the GSK-3β group than the LacZ group. Moreover, lowest myocardial infarction size was found in the GSK-3β group (P < 0.05). All these experimental findings show that GSK-3 overexpression plays a positive role in promoting the therapeutic effect of cardiac stem cell transplantation.     

睾酮对大鼠心肌梗塞后心肌肥大的影响

本文应用立体形态定量技术,观察睾酮(T)对心肌梗塞后心肌肥大的影响。实验分为:假手术组(S组)、心肌梗塞组(MI组)。心肌梗塞后睾酮治疗组(MIT组)。结果证明,与S组相比,MI及MIT组大鼠心肌细胞核密度明显减少,尤其以MIT组变化显著,MIT组平均核长度明显增加;MI组的 dp/dt max明显降低,T值延长,MIT组的上两指标无显著差异。MI后血浆T总浓度与平均每核心肌细胞体积呈显著正相关关系。提示:睾酮确实促进了MI后心肌肥大,从而促进了心功能的恢复。     

Long-term administration of tempol attenuates postinfarct ventricular dysfunction and sympathetic activity in rats

The purpose of this study was to determine whether the long-term administration of tempol attenuates postinfarct ventricular dysfunction and sympathetic activity in rats. Myocardial infarction (MI) was induced by left descending coronary artery ligation. Tempol was orally administered in drinking water (2 mmol/L), which was initiated 4 h after infarction and continued for 6 weeks. Tempol prevented not only the increases in left ventricular end-diastolic pressure and volume but also the decreases in ejection fraction and peak velocities of contraction in MI rats. The treatment normalized the increased renal sympathetic nerve activity (RSNA) and plasma norepinephrine level, as well as the enhanced cardiac sympathetic afferent reflex (CSAR; an excitatory cardiovascular reflex partially contributing to the sympathetic activation in chronic heart failure) and the RSNA responses to microinjection of angiotensin II into paraventricular nucleus in MI rats. Furthermore, tempol prevented the increased AT₁ receptor protein expression and superoxide anion level in both paraventricular nucleus and rostral ventrolateral medulla in MI rats. In conclusion, long-term administration of tempol attenuates ventricular dysfunction and normalizes sympathetic neural control in MI rats. The normalization of the CSAR, levels of superoxide anions and AT₁ receptor expression, and the response to angiotensin II in the paraventricular nucleus and rostral ventrolateral medulla may partially contribute to the beneficial effects of tempol on central sympathetic control.     

The effect of beta-blockade on myocardial remodelling in Chagas' cardiomyopathy

OBJECTIVE:

Chagas'' disease has spread throughout Latin America because of the high rate of migration among these countries. Approximately 30% of Chagas'' patients will develop cardiomyopathy, and 10% of these will develop severe cardiac damage leading to heart failure. Beta-blockade improves symptoms and survival in heart failure patients; however, its efficacy has not been well established in Chagas'' disease. We evaluated the role of carvedilol in cardiac remodeling and mortality in a Chagas'' cardiomyopathy animal model.

METHODS:

We studied Trypanosoma cruzi infection in 55 Syrian hamsters that were divided into three groups: control (15), infected (20), and infected + carvedilol (20). Animals underwent echocardiography, electrocardiography, and morphometry for collagen evaluation in ventricles stained with picrosirius red.

RESULTS:

The left ventricular diastolic diameter did not change between groups, although it was slightly larger in infected groups, as was left ventricular systolic diameter. Fractional shortening also did not change between groups, although it was slightly lower in infected groups. Collagen accumulation in the interstitial myocardial space was significantly higher in infected groups and was not attenuated by carvedilol. The same response was observed in the perivascular space. The survival curve showed significantly better survival in the control group compared with the infected groups; but no benefit of carvedilol was observed during the study. However, in the acute phase (up to 100 days of infection), carvedilol did reduce mortality.

CONCLUSION:

Carvedilol did not attenuate cardiac remodeling or mortality in this model of Chagas'' cardiomyopathy. The treatment did improve survival in the acute phase of the disease.     

Hyperhomocysteinemia inhibited cardiac stem cell homing into the peri-infarcted area post myocardial infarction in rats

Background

Hyperhomocysteinemia (HHcy) has been reported as an independent risk factor for coronary artery disease; however it is not clear regarding the action of HHcy on the homing of cardiac stem cells (CSCs) to the damaged myocardium and the consequent CSCs-mediated cardiac repair post myocardial infarction.

Methods

Sprague–Dawley (SD) rats were divided into 4 groups. HHcy was induced in the rats by a 6-week high-methionine diet. Rat heart MI model was developed by left coronary artery ligation. Immunofluorescence was used to examine the CSCs migration in vivo via injecting BrdU-labeled CSCs into AV-groove followed by a coronary ligation. Immunohistochemistry, western blot and ELISA analysis were carried out to detect the expression of stem cell factor (SCF) protein, and RT-PCR was conducted for the expression of SCF mRNA.

Results

On day 5 of MI model creation, accumulation of CSCs was significantly increased in the peri-infarcted area by the non-hyperhomocysteinemic rats, which led to an improvement of cardiac function at 3 weeks after MI. however, the accumulation of CSCs was markedly decreased by the hyperhomocysteinemic rats followed with the decline of cardiac function. SCF expression was also significantly decreased in the peri-infarcted area by the hyperhomocysteinemic rats compared to the non-hyperhomocysteinemic rats. The experiments in vitro confirmed that homocysteine (Hcy) decreased SCF expression via inhibition of TNF-α-induced activity of NF-κB, further reduced the migration of CSCs.

Conclusion

It demonstrated that hyperhomocysteinemia may significantly contribute to restrain CSCs-mediated cardiac repair by reducing SCF-induced homing of CSCs.     

芪苈强心对心肌梗死后大鼠心肌细胞凋亡的影响

目的: 探讨芪苈强心对心肌梗死大鼠心肌细胞凋亡的影响。方法: 结扎冠脉前降支制作大鼠心肌梗死模型,随机分为假手术组(sham, n=5)、心肌梗死组(MI, n=16)和芪苈强心组(4 g·kg^-1·d^-1, n=15),28 d后检测心肌梗死面积,TUNEL法检测心肌细胞凋亡指数(AI),免疫组化法检测Fas蛋白表达,Western blotting检测黄嘌呤氧化酶(XO)和caspase-3蛋白表达,比色法测定XO和清除活性氧活性。结果: MI组非梗死区心肌细胞AI升高,Fas、XO和caspase-3蛋白表达增强,XO活性增加,清除活性氧活性降低(P<0.01)。芪苈强心组与MI组比较,非梗死区心肌细胞AI降低,Fas和caspase-3蛋白表达减少,XO活性降低,清除活性氧活性升高(P<0.01),但梗死面积和XO蛋白表达在两组间无显著差异(P>0.05)。结论: 芪苈强心能够抑制非梗死区心肌细胞凋亡,其作用机制可能与减少活性氧簇生成及降低Fas和caspase-3的表达有关。     

Swimming exercise training prior to acute myocardial infarction attenuates left ventricular remodeling and improves left ventricular function in rats

The effect of exercise training prior to acute myocardial infarction (AMI) on left ventricular (LV) remodeling is poorly understood. This study investigated the protective effect of 3 weeks of swimming exercise training prior to AMI on cardiac morphology and function. Male Sprague-Dawley rats (n = 35) were randomly assigned to 3 groups: swimming training (n = 14, 90 min, 5 days/wk, 3 wk), sedentary (n =14), and controls (n = 7, no exercise, no MI). At the end of the training/sedentary period, rats were subjected to AMI (ExMI and SedMI) induced by surgical ligation of the left coronary artery. Thereafter, the rats remained sedentary for a 4-wk recovery period. Trans-thoracic echocardiography was performed in each group at the end of the exercise/sedentary period (pre-AMI), 24 hr after AMI, and following recovery (4 wk after AMI). No differences were observed in LV dimensions and function pre-AMI among the 3 groups; however, LV-end systolic diameter (LVESD) and LV-end systolic area (LVES-area) were significantly lower in the prior trained rats, 24 hr post-AMI with no additional change 4 wk post-AMI, during remodeling. Both LV-shortening fraction (SF%) and fractional area change (FAC%) were higher in the trained animals 4 wk post-AMI (39+/-12% vs 23+/-8%; p 0.002, and 48+/-14% vs. 38+/-9%; p 0.07, respectively). In conclusion, 3 wk of swimming exercise training prior to AMI significantly attenuated LV remodeling and improved LV function, despite no changes in LV dimensions or systolic function at the end of the exercise session. The data suggest that even a short-term training period is sufficient to induce cardiac protection.     

Exercise training attenuates acute hyperalgesia in streptozotocin-induced diabetic female rats

OBJECTIVES:

We investigated the effects of chronic (eight weeks) low- to moderate-intensity swimming training on thermal pain sensitivity in streptozotocin-induced diabetic female rats.

METHODS:

Female Wistar rats (n = 51) were divided into the following groups: trained streptozotocin-induced diabetic rats [hyperglycemic trained (HT)], sedentary streptozotocin-induced diabetic rats [hyperglycemic sedentary (HS)], normoglycemic trained rats (NT) and normoglycemic sedentary rats (NS). Diabetes was induced by a single injection of streptozotocin (50 mg/kg, i.p.). One day after the last exercise protocol (60 min/day, five days/week for eight weeks) in the trained groups or after water stress exposure (ten min/twice a week) in the sedentary groups, the rats were subjected to a hot plate test.

RESULTS:

After eight weeks of swimming training, streptozotocin-induced diabetic rats presented a significantly lower body mass (trained: 219.5±29 g, sedentary: 217.8±23 g) compared with the normoglycemic groups (trained: 271±24 g, sedentary: 275.7±32 g). Interestingly, we did not find differences in blood glucose levels (mg/dl) between the trained and sedentary groups of the hyperglycemic or normoglycemic rats (HT: 360.2±66.6, HS: 391.7±66.7, NT: 83.8±14.0, NS: 77.5±10.1). In the hot plate test, the rats from the HT group presented a significantly lower latency than the other rats (HT: 11.7±7.38 s, HS: 7.02±7.38 s, NT: 21.21±7.64 s, NS: 22.82±7.82 s).

CONCLUSION:

Low-to-moderate swimming training for a long duration reduces thermal hyperalgesia during a hot plate test in streptozotocin-induced diabetic female rats.     

Qiliqiangxin improves cardiac function and attenuates cardiac remodeling in rats with experimental myocardial infarction

Objective: It has been reported that Qiliqiangxin (QL), a traditional Chinese medicine compound, could inhibit cardiac hypertrophy and remodeling, and improve cardiac function. However, whether and how it reverses cardiac remodeling in rats post myocardial infarction (MI) remains unknown. This study aims to explore related mechanisms linked with cardiac function improvement and attenuation of cardiac remodeling by QL in rats with experimental MI. Methods: MI was induced by ligation of left anterior descending coronary artery (LAD) in male Sprague-Dawley rats. Rats with LVEF < 50% at four weeks after procedure were treated for another 6 weeks with placebo, QL and captopril. Echocardiography and plasma NT-proBNP were measured at the end of study, and histological studies were performed. Protein expressions of Neuregulin-1 (NRG-1), total-Akt, phospho-Akt (Ser473), hydroxy-HIF-1α (Pro564), VEGF, Bax, Bcl-2 and Caspase 3 were examined by Western blot. mRNA expression of NRG-1 and p53 was detected by real-time PCR. Results: Compared with the placebo group, QL improved cardiac function, reduced left ventricular dimension, inhibited interstitial inflammation and fibrosis, increased neovascularization, and attenuated cardiomyocyte apoptosis. Meanwhile QL significantly upregulated the expression of HIF-1α, VEGF, enhanced phosphorylation of Akt, decreased the ratio of Bax/Bcl-2 and Caspase 3 expression. Furthermore, we observed upregulation of NRG-1 and downregulation of p53 after QL treatment. Conclusion: Our data suggest that the beneficial effects of QL on improving cardiac function and attenuating cardiac remodeling post MI are associated with angiogenesis enhancement and apoptosis inhibition, which may be mediated via activation of NRG-1/Akt signaling and suppression of p53 pathway.     

肝素缓释支架置入急性心肌梗死患者后的血管再生及心肌功能改善

背景：采用裸金属支架置入治疗心肌梗死可在一定程度上改善心肌功能,但容易出现血栓等情况。目的：分析肝素缓释支架对急性心肌梗死后患者血管再生及心肌功能改善的影响。方法：纳入急性心肌梗死患者87例,其中男47例,女40例,年龄55-81岁,分两组治疗,观察组(n=45)经皮冠状动脉置入肝素缓释支架,对照组(n=42)经皮冠状动脉置入裸金属支架。随访12个月,观察两组血管再生、心肌功能改善及心脏不良事件发生情况。结果与结论：观察组新生血管密度A值、心肌存活面积A值、左心室射血分数均高于对照组(P < 0.05);随访3个月时,观察组有1例出现再次血运重建,1例出现急性复发心肌梗死;对照组有1例患者出现再次血运重建,1例出现急性复发心肌梗死,1例出现心脏性死亡,两组心脏不良反应情况比较差异无显著性意义。表明经皮冠状动脉置入肝素缓释支架治疗急性心肌梗死可有效促进血管再生,改善心肌功能,并具有良好的生物相容性。中国组织工程研究杂志出版内容重点：生物材料;骨生物材料; 口腔生物材料; 纳米材料; 缓释材料; 材料相容性;组织工程     

心肌梗塞后泵功能的恢复及其机制的实验研究

造成大鼠不同范围的心肌梗塞(MI)后,动态观察不同时期的静息和容量负荷状态下泵功能恢复的规律及其代偿机制。结果证明:(1)梗塞范围(IS)小于左室的46%时,泵功能都有自动恢复的可能性。IS越小,恢复越快、越好。IS超过46%时未见恢复;(2)在IS相同的条件上,静息状态的泵功能远较负荷状态的泵功能恢复得好;(3)MI后,泵功能代偿机制的代偿效应与IS呈反比。如IS超过46%,任何代偿机制均难以发挥效应。     

Heart-type fatty acid binding protein as an adjunct to cardiac troponin-I for the diagnosis of myocardial infarction

We hypothesized that when used in combination with cardiac troponins, heart-type fatty acid binding protein (H-FABP) would have greater diagnostic value than conventional markers for the early diagnosis of myocardial infarction (MI). Patients with typical chest pain at a single emergency department were consecutively enrolled. Initial blood samples were drawn for H-FABP, myoglobin, creatine kinase isoenzyme MB (CK-MB), and cardiac troponin-I (cTnI) measurements. MI was defined by serial cTnI measurements. To evaluate the adjunctive role of biochemical markers, we derived and compared logistic regression models predicting MI in terms of their discrimination (area under the receiver operating characteristics curve, AUC) and overall fit (Bayesian information criterion, BIC). Seventy-six of 170 patients were diagnosed as having MI. The AUC of cTnI, H-FABP, myoglobin, and CK-MB were 0.863, 0.827, 0.784, and 0.772, respectively. A logistic regression model using cTnI (P = 0.001) and H-FABP (P < 0.001) had the biggest AUC (0.900) and the best fit determined by BIC. Sensitivity, specificity, positive likelihood ratio, and negative likelihood ratio of this model at 30% probability were 81.6%, 80.9%, 4.26, and 0.23, respectively. H-FABP has a better diagnostic value than both myoglobin and CK-MB as an adjunct to cTnI for the early diagnosis of MI.     

高血压与2型糖尿病协同作用导致小鼠心功能障碍和心肌重塑

目的:研究高血压与2型糖尿病联合作用是否能导致小鼠心功能障碍和心肌重塑。方法:将14周龄的2型糖尿病和非糖尿病小鼠经血管紧张素Ⅱ(Ang Ⅱ)给药4周诱导小鼠形成轻度高血压。运用超声波心动描记术和多巴酚丁胺负荷试验评价小鼠左心室功能;HE染色分析左心室心肌细胞的肥大作用;Western blotting测定心肌组织中磷酸化腺苷酸活化蛋白激酶(p-AMPK)的表达水平。结果:与非糖尿病小鼠比较,糖尿病小鼠(DM组)的心脏功能和心肌结构无明显变化;Ang Ⅱ给药不影响2型糖尿病小鼠和非糖尿病小鼠的体重和血糖含量,但血压明显增高;左心室重量和心肌细胞表面积结果分析显示,Ang Ⅱ诱导2型糖尿病小鼠的左心室肥大程度显著大于Ang Ⅱ组;Ang Ⅱ给药的2型糖尿病小鼠左心室的缩短分数和射血分数显著降低,而Ang Ⅱ组小鼠无明显变化;Western blotting结果显示Ang Ⅱ组、DM组和DM+Ang Ⅱ组小鼠左心室组织中p-AMPK的表达量显著降低。结论:2型糖尿病小鼠心脏功能和心肌结构无明显变化,当高血压存在时2型糖尿病小鼠容易发生心脏功能障碍和心肌重塑,提示高血压是2型糖尿病小鼠心脏功能障碍和心肌重塑的关键因子。