Effect of carvedilol on cardiac function and left ventricular remodeling in rats after acute myocardial infarction

Objective: To observe the effect of carvedilol injection on left ventricular function and collagen remodelingin rat with myocardial infarction. Methods: Sixty rats with a model of myocardial infarction were randomly divided intonine groups. The rats of therapeutical group were treated with carvedilol injection (2 mg/d intraperitoneal injection)and/or captopil (2 g/L drinking water). Acute myocardial infaction (AMI) group did not receive drug treatment. Theanimals were sacrificed at 4 weeks and 8 weeks after coronary artery ligation. The levels of plasma angiotensin Ⅱ andplasma aldosterone and left ventricle function were determined at different time. The collagen content and the raio of     

卡维地洛对家兔急性心肌梗死左室重构的作用

目的评价第三代β-受体阻滞剂卡维地洛对家兔急性心肌梗塞(AMI)后的左室重构的防治作用,以及对梗死区损伤心肌细胞的修复.方法采用家兔制备心肌梗死模型,20只AMI术后成活的雄性家兔随机分为AMI对照组、卡维地洛(CVD)组,另设假手术组.灌胃给药4周后处死动物.用电子精确天平称量左室、右室的重量,用羟脯氨酸方法测定心肌组织的胶原的含量及采集标本进行病理分析.结果梗死后左心室、右心室重量均比假手术组增加,差异显著.梗死区胶原含量显著增加,非梗死区胶原含量增加明显.经卡维地洛治疗后,左心室、右心室重量均下降,但未能恢复至正常水平.梗死区胶原含量亦略有下降,但差异不显著.非梗死区胶原含量下降明显,差异显著.病理分析结果显示卡维地洛组心肌细胞损伤程度减轻.结论卡维地洛能有效防治家兔AMI后的左室重构及减轻心肌细胞损伤程度.     

卡维地洛对兔心肌梗死后转化生长因子β1表达和心室重构的影响

目的探讨卡维地洛对兔心肌梗死后转化生长因子β1（TGF-β1）的表达和心室重构的影响。方法采用结扎冠状动脉左室支建立心肌梗死（MI）模型（假手术组开胸后在相应部位挂线不结扎）。术后24h将存活兔分为3组：假手术组、MI组、MI＋卡维地洛组。各组饲养4周后行血流动力学检查;测量体质量,左、右心室重量;采用苦味酸-酸性品红（VG）染色检测非梗死区的胶原容积分数（CVF）;采用免疫组化检测TGF-β1的表达情况。结果MI组与假手术组比较,左心室重量/体质量值（RVW/BW）、右心室重量/体质量（LVW/BW）、左室舒张末压（LV-EDP）、非梗死区CVF均显著升高（P〈0.05或P〈0.01）,TGF-β1的表达显著增强（P〈0.01）;MI＋卡维地洛组与MI组比较,RVW/BW、LVEDP、CVF均显著降低（P〈0.05或P〈0.01）,TGF-β1表达明显减弱（P〈0.05）。结论TGF-β1可能与心肌梗死后心室重构有关;卡维地洛能缓解心肌梗死后非梗死区的重构,其机制可能与减低TGF-β1的表达有关。     

卡维地洛对急性心肌梗死大鼠心肌细胞外基质重塑的影响

目的:研究卡维地洛对急性心肌梗死(AMI)后大鼠心肌细胞外基质(ECM)重塑的影响。方法:在体结 扎Wistar大鼠冠状动脉左前降支建立AMI模型,存活24h者随机分为卡维地洛治疗组(n=11)和AMI组(n= 12),另以仅穿线不结扎左前降支建立假手术组(n=10)。卡维地洛治疗组给予卡维地洛10mg/(kg·d)灌胃,2 次/d;AMI组和假手术组仅给予同体积生理盐水灌胃,2次/d。4周末用半定量RT PCR法检测各组大鼠左室心肌 非梗死区基质金属蛋白酶MMP- 2和MMP 9mRNA表达,采用明胶酶谱法测定2者活性,采用苦味酸 酸性品红染 色测定心肌总胶原,计算胶原容积分数(CVF)。结果:AMI组大鼠心肌非梗死区MMP 2、MMP -9mRNA表达及活 性,以及CVF均较假手术组增加(P<0.01),而卡维地洛治疗组上述指标均低于AMI组(P<0.01)。结论:卡维地 洛可改善心肌梗死后非梗死区心肌细胞外基质重塑,这可能是其对心肌梗死有益作用的机制之一。     

辛伐他汀对大鼠急性心肌梗死后心肌白细胞介素-6表达的影响

目的:观察辛伐他汀对大鼠急性心肌梗死(AMI)后心肌组织白细胞介素- 6 (IL -6)基因及其蛋白表达的影响。方法:Wistar大鼠随机分 3组:辛伐他汀治疗组(MI- S组)、梗死对照组(MI C组)和假手术组 (Sham组 )。前2组大鼠结扎左冠状动脉前降支(LAD)制成AMI模型,MI S组给辛伐他汀 40mg/kg灌胃治疗,余 2组给予生理盐水灌胃。4周后,RT- PCR法和免疫组织化学法分别检测左心室梗死及非梗死区IL- 6mRNA和蛋白的表达,Westernblot法测定左心室非梗死区心肌IL- 6蛋白表达。结果:大鼠AMI后 4周,MI C和MI S组左心室梗死及非梗死区心肌IL- 6mRNA及蛋白表达均较Sham组明显升高(P<0. 05),MI S组IL- 6mRNA及蛋白表达均较MI C组低 (P<0. 05)。3组血脂差异无统计学意义。结论:辛伐他汀可减少AMI大鼠左心室心肌IL 6mRNA及蛋白表达,此改变不依赖其降脂作用。     

细胞周期蛋白A2在大鼠急性心肌梗死后心肌细胞的表达

目的:探讨急性心肌梗死后梗死区周围心肌细胞内细胞周期蛋白A2(cyclin A2)的表达?方法:制作SD大鼠急性心肌梗死模型,分别于梗死后3d?1周?2周?3周?4周各处死5只大鼠,5只假手术大鼠为对照,取出心脏组织,进行Masson染色,同时使用免疫组织化学法检测心脏组织中cyclin A2及磷酸化组蛋白H3(phospho-histone H3,H3P)的表达?结果:Masson染色从病理上证明心肌梗死模型构建成功;梗死区周围心肌细胞cyclin A2的表达在梗死后1周时最高,阳性细胞染色百分比为(7.72 ± 1.16)%,2周后逐渐下降,梗死后4周时,与假手术组相似,几乎无阳性表达?梗死后第3天?1周?2周和3周均可见少量心肌细胞核表达H3P,其阳性率为1.56%~3.12%?结论:心肌细胞cyclin A2的阳性表达提示急性心肌梗死后梗死区周围少部分心肌细胞能重新进入有丝分裂周期?     

阿托伐他汀对大鼠缺血心肌TRAIL表达及细胞凋亡的影响

目的:观察阿托伐他汀对大鼠缺血心肌肿瘤坏死因子相关凋亡诱导配体(TRAIL)表达的影响,以及与心肌细胞凋亡和凋亡相关基因Bax、Bcl-2的关系,探讨TRAIL因子在心血管疾病中所起的作用。方法:采用左冠状动脉结扎的方法建立大鼠心肌梗死模型。健康雄性SD大鼠随机分为三组:假手术组、心梗组、阿托伐他汀(10 mg.kg-1.d-1)组。全自动生化分析仪检测血脂水平;病理组织学测定心肌梗死面积;免疫组化及实时定量RT-PCR测定心肌TRAIL、Bax、Bcl-2的表达;TUNEL法测定心肌细胞凋亡。结果:与假手术组相比,心梗组凋亡细胞数显著增加;与心梗组相比,阿托伐他汀组心肌细胞凋亡数显著减少(P<0.01)。与假手术组相比,心梗组Bcl-2/Bax下降;与心梗组相比,阿托伐他汀组Bcl-2/Bax明显上调(P<0.05)。与假手术组相比,心梗组TRAIL在蛋白及基因水平表达明显下降;与心梗组相比,阿托伐他汀组心肌TRAIL蛋白表达显著升高(P<0.01)。结论:阿托伐他汀促使大鼠缺血心肌TRAIL基因表达上调,TRAIL基因可能参与了阿托伐他汀抗心肌细胞的凋亡过程。     

The beta-adrenergic blocker carvedilol restores L-type calcium current in a myocardial infarction model of rabbit

Background Carvedilol, an antagonist of α1- and β-adrenergic receptors, has shown efficacy in reducing all-cause death and arrhythmia death for ischemic heart disease and congestive heart failure in several large-scale trials. It has been found to prevent ventricular remodeling, and recently was reported to reverse down-regulation of Na+ channel in a chronic heart failure model. This study was conducted to investigate whether carvedilol could reverse the ion remodeling in a myocardial infarction model of rabbit.Methods After the procedure of coronary ligation, animals were randomized to placebo or carvedilol treatment (5 mg/kg). Action potentials, L-type calcium current (Ica L) and the effect of isoproterenol stimulation on Ica L were measured using whole-cell patch method. Evaluation of the expression of calcium channel subunits was carried out by RT-PCR and Western blot. Results The results indicate that mean peak Ica L densities (pA/pF) at +10 mV was reduced in postinfarction myocytes (5.33±0.45, n=25) compared to sham myocytes (6.52±0.21, n=20). Treatment of myocardial infarction rabbits with carvedilol could restore it partially (5.91±0.39, n=20, P&lt;0.05). However, steady-state activation parameters were similar in three groups. With stimulation by isoproterenol (1 μmol/L) Ica L increased in all three groups, but the increase was smaller in postinfarction myocytes. mRNA levels of calcium channel subunit CaA1 gene was decreased but CaB2a, CaB2b and CaB3 mRNA levels did not change after MI. Corresponding change in CaA1 protein was also observed. Conclusions The results demonstrate that carvedilol restores Ica L density and reverse the downregulation of CaA1 postinfarction.     

急性心肌梗死大鼠血管紧张素Ⅱ对PAI-1和tPA表达的作用及其机制

目的:探讨急性心肌梗死(AMI)大鼠血管紧张素Ⅱ(AngⅡ) 经AngⅡ1型受体(AT1R)激活细胞外信号调节激酶(ERK)对纤溶酶原激活物抑制剂-1(PAI-1)和组织型纤溶酶原激活物(tPA)活性的调节作用.方法:24只健康SD大鼠,按随机数字表法随机分为假手术组(n=8)、AMI组(n=8)和特异性ERK上游激酶...     

银丹心脑通软胶囊对大鼠急性心肌梗死后心肌组织中骨桥蛋白表达的影响及其心肌保护作用机制

目的：探讨银丹心脑通软胶囊对大鼠急性心肌梗死（AMI）后心肌组织中骨桥蛋白（OPN）表达的影响,阐明银丹心脑通软胶囊改善大鼠AMI的作用机制。方法：将90只Wistar大鼠结扎冠脉前降支建立AMI模型,术后存活动物随机分为模型组、银丹心脑通软胶囊小剂量组（银丹心脑通软胶囊0.8 g/kg/d）、银丹心脑通软胶囊大剂量组（银丹心脑通软胶囊1.6 g/kg/d ）、阳性药卡托普利组（卡托普利5 g/kg/d）,每组12只,同时设假手术组(只穿线不结扎)(n=10),连续给药4周。HE和Masson染色观察各组大鼠心肌组织学表现;脱氧核苷酸末端转移酶介导的缺口末端标记法（TUNEL） 原位检测凋亡细胞的DNA碎片,计算凋亡指数（AI）;RT-PCR法检测非梗死区心肌中OPN mRNA表达水平。结果：与假手术组比较,模型组大鼠AI明显升高(P<0.05);与模型组比较,各给药组大鼠AI明显降低（P<0.01）;与卡托普利组比较,银丹心脑通大剂量组大鼠AI明显降低,差异有统计学意义(P<0.05),银丹心脑通小剂量组大鼠AI无明显改变(P>0.05)。RT-PCR检测,与假手术组比较,模型组大鼠左心室非梗死区心肌组织中OPN mRNA表达水平明显升高(P<0.01);与模型组比较,各给药组大鼠左心室非梗死区心肌组织中OPN mRNA表达水平明显降低（P<0.01）;与卡托普利组比较,银丹心脑通大剂量组大鼠左心室非梗死区心肌组织中OPN　mRNA表达水平明显降低(P<0.05),而银丹心脑通小剂量组OPN　mRNA表达水平无明显改变（P>0.05）。结论：银丹心脑通软胶囊能够显著改善心肌梗死后大鼠心肌组织细胞凋亡,降低左心室非梗死区OPN mRNA表达水平,提示银丹心脑通软胶囊对大鼠AMI的心肌保护作用可能与降低OPN mRNA表达有关。     

卡维地洛防治急性心肌梗死后左心室重构的临床研究

目的:为比较卡维地洛与卡托普利防治急性心肌梗死(AMI)后左心室重构的效果.方法:将122名AMI患者随机分为卡维地洛组52例,卡托普利组50例,常规治疗组20例,分别于治疗后1周、6个月采用心脏多普勒超声测定室间隔厚度(IVST)、左室后壁厚度(LVPWT)、左室舒张末内径(LVDd),计算左室重量指数(LVMI),同时测定左室射血分数(LVEF)及舒张早期左室充盈最大速率(E峰)与心房收缩期最大速率(A峰).结果:卡维地洛组和卡托普利组与常规治疗组比较均可使IVST、LVPWT变薄(P＜0.01),LVDd缩小(P＜0.01),LVMI降低(P＜0.01).卡维地洛组和卡托普利组均可增加LVEF、降低A/E峰比值,与常规治疗组比较1周时P＜0.05,6个月时P＜0.01.结论:卡维地洛具有良好的防治AMI后左室重构效果.     

抑郁对心肌梗死大鼠缺血心肌细胞凋亡及Bcl-2、Bax和Caspase-3表达的影响

目的:探讨抑郁对心肌梗死大鼠缺血心肌细胞凋亡及Bcl-2、Bax和Caspase-3的影响。方法:大鼠随机分为四组,各组8只,A组为假手术组,B组为抑郁大鼠假手术组,C组为心肌梗死组,D组为抑郁大鼠心肌梗死组。用TUNEL法检测心肌细胞凋亡,用免疫组织化学法和逆转录-聚合酶链反应方法检测Bcl-2、Bax和Caspase-3的基因表达。结果:各组大鼠心肌细胞凋亡指数以及心肌细胞Bcl-2、Bax、Caspase-3蛋白表达和心肌细胞Bcl-2、Bax、Caspase-3 mRNA表达的差异有统计学意义(P<0.01),C、D组大鼠心肌细胞凋亡指数以及心肌细胞Bcl-2、Bax、Caspase-3蛋白表达和心肌细胞Bcl-2、Bax、Caspase-3 mRNA表达均高于A组和B组,差异有统计学意义(P<0.01),D组大鼠心肌细胞凋亡指数以及心肌细胞Bax、Caspase-3蛋白表达和心肌细胞Bax、Caspase-3 mRNA表达高于C组,而心肌细胞Bcl-2蛋白及mRNA表达低于C组,差异有统计学意义(P<0.05)。结论:抑郁可以加重心肌梗死大鼠缺血心肌细胞凋亡,其机制可能与上调促凋亡基因Bax及Caspase3表达、下调抗凋亡基因Bcl-2的表达有关。     

miR-126对急性心肌梗死大鼠心肌细胞凋亡的影响

目的探讨miR-126对急性心肌梗死(AMI)大鼠心肌细胞凋亡的影响。方法通过冠状动脉左前降支结扎大鼠建立AMI模型,随机分为AMI组、miR-126 mimics negative control(NC)组及miR-126组,其中NC组及miR-126组分别采用心肌组织局部注射慢病毒转染miR-126 mimics NC及miR-126 mimics,另外假手术组采用冠状动脉左前降支穿线不结扎。记录大鼠心脏功能,TCC法及原位末端凋亡法(TUNEL)检测心肌凋亡指数及梗死面积,比色法检测天冬氨酸蛋白水解酶(Caspase 3)及Caspase 8活性,Western-blot法检测Bax及Bcl-2表达,同时RTPCR法检测Fas及Fas-L mRNA表达。结果与假手术组比较,AMI组及NC组左室射血分数(LVEF)及左室长轴缩短分数(FS)升高,左室舒张末期内径(LVDd)及左室收缩末期内径(LVDs)降低,心肌凋亡指数提高,心肌梗死面积增大,Caspase 3及Caspase 8活性上升,Bax蛋白表达量上调,Bcl-2蛋白表达量下调,Fas及Fas-L mRNA水平上升,差异具有统计学意义(P0.01)。与AMI组及NC组比较,miR-126组能扭转此变化,差异具有统计学意义(P0.01)。结论 miR-126能显著抑制AMI大鼠心肌细胞凋亡,与调节细胞凋亡相关蛋白表达有关。     

卡维地洛与倍他乐克防治大鼠AMI左室重构作用的比较

目的对比卡维地洛及倍他乐克对大鼠急性心肌梗死(AMI)左室重构(LVRM)的防治作用.方法 105只AMI术后成活的雌性SD大鼠随机分成AMI对照(n=35)、卡维地洛1 mg/(kg@d)(n=35)和倍他乐克2 mg/(kg@d)(n=35)三组.另设假手术组.给药4周后行血流动力学测定和病理分析.去除死亡及梗死面积＜35%或＞55%者,最终46只大鼠资料完整,在以上各组分别为11,12,11和12只.结果与假手术组相比,AMI组的左室舒张末压(LVEDP)、容积(LVV)、重量(LVW)显著增加(P＜0.05～0.111),左室内压最大上升和下降速率(±dp/dt)及其校正值(±dp/dt/LVSP)显著降低(P＜0.01～0.001).与AMI组相比,卡维地洛和倍他乐克组的LVEDP及LVV均显著降低(P均＜0.001),±dp/dt及±dp/dt/LVSP均显著升高(P＜0.05～0.001),而LVW和RVW仅在卡维地洛组显著减轻(P均＜0.05～0.01).结论 1、卡维地洛能有效抑制大鼠AMI左室重构并改善血流动力学和左室功能,2、倍他乐克与卡维地洛的作用相似,但对心室肥厚似无抑制作用.     

Huoxue Anxin Recipe(活血安心方)Promotes Myocardium Angiogenesis of Acute Myocardial Infarction Rats by Up-Regulating miR-210 and Vascular Endothelial Growth Factor

Objective: To investigate the microR NAs(miR NAs) expression profile of acute myocardial infarction(AMI) rats and the regulating effects of Huoxue Anxin Recipe(活血安心方, HAR) on angiogenesis-related miR NAs and genes. Methods: Forty-five Wistar rats were randomly assigned to 3 groups according to a random number table: sham, AMI, and AMI+HAR groups(15 in each group). AMI rats were established by ligation of the left descending coronary artery. HAR was intragastrically administered to rats of the AMI+HAR group for successive 21 days since modeling, meanwhile the same volume of 0.9% normal saline was administered to rats of the sham and AMI groups. Doppler echocardiography was used for noninvasive cardiac function test. Hematoxylin and eosin staining was used to observe the histopathological change. miR NAs expression profile was detected by quantitative realtime polymerase chain reaction(qR T-PCR). The mR NA and protein expressions of vascular endothelial growth factor(VEGF), and a target gene of miR-210 was further detected by qR T-PCR and Western blot, respectively. The microvessels density of myocardium was evaluated by CD31 immunostaining. Results: Compared with the sham group, ejection fraction(EF) and fractional shortening(FS) values were decreased significantly in the AMI group(P0.01), while the infarction area and the interstitial collagen deposition were increased obviously. As for the AMI+HAR group, EF and FS values were increased significantly(P0.05 vs. AMI group), and the infarction area was reduced and the interstitial collagen deposition were alleviated significantly. Total of 23 miR NAs in the AMI group expressed differently by at least 1.5 folds compared with those in the sham group; 5 miR NAs in the AMI+HAR group expressed differently by at least 1.5 folds compared with those in the AMI group. Among them, miR-210 was low in the AMI group and high in the AMI+HAR group. The relative mR NA and protein expressions of VEGF were decreased significantly in the AMI group(P0.05 vs. sham group), and increased significantly in the AMI+HAR group(P0.01 vs. AMI group). CD31 expression area and optical intensity were decreased significantly in the AMI group(P0.05 vs. sham group), and increased significantly in the AMI+HAR group(P0.01 vs. AMI group). Conclusions: HAR could reduce the infarction area, alleviate the interstitial fibrosis and improve the cardiac function of AMI rats. Those effects could be related to promoting myocardium angiogenesis of HAR by up-regulating miR-210 and VEGF.     

冠心合剂对急性心梗大鼠心肌bFGF表达及血管新生的影响

目的：观察冠心合剂对急性心肌梗死（AMI）大鼠碱性成纤维生长因子（basic fibroblast growth factor,bFGF）表达及血管新生作用的影响及作用机制。方法：SD大鼠65只,除假手术组8只外,其余大鼠结扎冠状动脉左前降支建立大鼠急性心肌梗死模型,造模成功40只。随机分为冠心合剂大、中、小剂量组及阳性对照组、模型组,各8只。造模后冠心合剂治疗组应用相应剂量冠心合剂灌胃,阳性对照组结扎后立即在结扎处周围喷洒1揿bFGF（125AU）,术后5天皮下注射肝素1 250 U/kg 1次;假手术组及模型组每天给予同等体积蒸馏水灌胃。术后2周处死各组大鼠,取心脏标本,HE染色,免疫组化方法显微镜下定量分析心肌bFGF蛋白表达,并根据VIII因子染色结果计算缺血心肌微血管密度（MVD）。结果：冠心合剂治疗组及阳性对照组大鼠心肌bFGF蛋白表达与新生微血管密度显著增加,明显高于模型组和假手术组（P〈0.01）;随冠心合剂剂量的增加,心肌梗死面积逐渐减小,心肌bFGF蛋白水平相应升高,心肌梗死边缘微血管密度逐渐增大;冠心合剂大剂量组疗效与阳性对照组相似（P〉0.05）。结论：冠心合剂可以增加急性心肌梗死（AMI）大鼠梗死区心肌bFGF蛋白表达和微血管密度,同时减少梗死面积,呈一定的剂量依赖性;冠心合剂促AMI大鼠血管新生的机制可能与增加心肌bFGF蛋白表达有关。     

High-frequency ultrasound evaluation of effects of early treatment with metoprolol on myocardial inflammatory cytokine expression in rats with acute myocardial infarction

This study evaluated the effects of early treatment with β-adrenergic blocker metoprolol on ventricular remodeling and function after acute myocardial infarction (AMI) by using high frequency ultrasound.The relationship between the efficacy and the expression level of cardiac myocardial inflammatory cytokine was examined in rats.The rat model of AMI was induced by ligating the left ante-rior descending artery.The surviving rats were randomly assigned to two experimental groups:MI control (MI) group and MI metoprolol (MI-B) group,with the rats undergoing sham operation serving as normal control (Sham).MI-B group was given metoprolol for 4 weeks (refer to the CCS-2 protocol) and the other two groups received equal volume of saline via intragastric (i.g.) administation.The ventricular remodeling and function were evaluated by high frequency ultrasound 4 weeks after the treatment.Then all rats were sacrificed for pathological examination and immunohistochemistrical detection of inflammatory cytokines,including IL-1β,IL-6,IL-10 and TNF-α.Compared with the MI group,the left ventricular end-systolic dimension,end-diastolic dimension,end-systolic volume and end-diastolic volume of the MI-B group were significantly decreased (P<0.01),while the left ventricular anterior wall end-diastolic thickness,ejection fraction and fractional shortening were obviously increased (P<0.01).The conspicuous improvement in the left ventricular morphology and function was coincident with the markedly reduced TNF-α and IL-1β expression and the increased IL-10 expression.We are led to conclude that early metoprolol treatment for AMI can regulate myocardial inflammatory cytokine expression to improve cardiac function and the underlying mechanism might be that it decreases the level of pro-inflammatory cytokines and increases the level of its anti-inflammatory counterparts in cardiac myocytes.Our study also showed that echocardiography is a useful technique for the structural and functional assessment of left ventricle after acute my     

糖尿病与非糖尿病患者合并急性心肌梗死的临床分析

目的探讨2型糖尿病（T2DM）与非糖尿病患者合并急性心肌梗死（AMI）的临床检测意义。方法以48例T2DM合并AMI为观察组,以80例非糖尿病合并AMI为对照组,对空腹血糖（FBG）、糖基化血红蛋白（HbAlc）、血脂、心肌酶学、射血分数（EF）水平变化,对两组并发心律失常、多部位心肌梗死、休克、胸痛及死亡率进行比较;同时比较胰岛素泵和多次注射胰岛素在糖尿病合并急性心肌梗死患者中的不同疗效,为T2DM合并AMI防治提供依据。结果T2DM组与非糖尿病组比较,两者在血糖、HbA,C、甘油三酯（TG）、胆固醇（CHOL）、心肌酶学、EF、心律失常、多部位心肌梗死、休克、胸痛及死亡率方面有显著差异（P〈O．05）,高密度脂蛋白（HDL_C）和低密度脂蛋白（LDL-C）无明显统计学差异（P〉o．05）;CSII组与MDII组相比,血糖更易控制,低血糖发生更少。结论T2DM组合并急性心肌梗死血糖、HbA,c、TG、CHOL、心肌酶学、心律失常、多部位心肌梗死、休克、胸痛及死亡率均高于非糖尿病组,心功能预后较非糖尿病组差;使用胰岛素泵患者血糖平稳下降,能更好控制血糖,保护残存心肌细胞。     

卡维地洛和美托洛尔对缺血再灌注损伤心肌细胞凋亡的影响

目的研究卡维地洛和美托洛尔对动脉粥样硬化家兔缺血再灌注损伤心肌细胞凋亡和脂质过氧化的影响。方法48只家兔随机分为4组（各组12只）：假手术组、模型组、美托洛尔组、卡维地洛组。采用高脂饮食并免疫损伤制作动脉粥样硬化模型,4周后给予药物,实验第8周时建立家兔心肌缺血再灌注模型。心电监护计数心率,测定家兔血脂指标（CH、TG）、超氧化物歧化酶（SOD）和丙二醛（MDA）,采用免疫组化的方法检测核因子-KBP65（NF-KBp65）及Fas蛋白的表达,采用末端标记原位细胞凋亡法检测心肌凋亡细胞。结果药物干预组心率较不用药组心率减慢（P〈O．01）。血清SOD水平模型组较假手术组明显降低（P〈O．01）,美托洛尔组和卡维地洛组血清SOD水平较模型组明显升高（P〈0．01）;卡维地洛组较美托洛尔组明显升高（P〈O．01）。模型组血清MDA水平、心肌细胞NF-闎、Fas蛋白表达和凋亡指数较假手术组明显升高（P〈0．01）,美托洛尔组和卡维地洛组各指标较模型组明显降低（P〈0．01）,卡维地洛组各指标较美托洛尔组明显降低（P〈0．01）。结论美托洛尔和卡维地洛均对缺血再灌注心肌细胞有保护作用,可能与它们抗氧化减轻脂质过氧化损伤,从而减少Fas和NF-kB蛋白的表达抗凋亡有关;卡维地洛对减少缺血再灌注心肌细胞凋亡方面优于美托洛尔。     

急性心肌梗死大鼠心肌组织p38的表达及其意义

目的探讨大鼠急性心肌梗死后不同时间点心肌组织中p38mRAN、p38蛋白的表达水平及意义。方法健康成年雄性SD大鼠36只,将其随机分为对照组、假手术组和心肌梗死模型组,模型组大鼠开胸结扎冠状动脉前降支以建立心肌梗死模型,成功结扎冠状动脉前降支后1、3、6、12h无痛处死大鼠并获取大鼠心肌组织;对照组大鼠不做任何处理;假手术组大鼠开胸冠状动脉穿线但不结扎冠状动脉;术后均无痛处死并获取心肌组织;分别采用RT-PCR、Western blot测定大鼠心肌组织p38mRNA及蛋白的表达水平。结果对照组与假手术组之间p38mRNA及蛋白表达的差异均无统计学意义(P>0.05);AMI组大鼠各亚组心肌组织中p38mRNA及蛋白表达均高于假手术组(P<0.05);AMI组中不同时间点亚组大鼠心肌组织中p38mRNA及蛋白的表达差异均有统计学意义(P<0.05),其表达量随结扎冠状动脉前降支时间的延长而增加,并于6h表达量达到高峰,随后下降,至12h其表达水平与假手术组差异无统计学意义(P>0.05)。结论 p38可能在心肌梗死后的病理过程中发挥作用。