不同剂量卡维地洛对心肌梗死后大鼠左室重构及心肌细胞凋亡的影响

目的观察不同剂量卡维地洛(CAR)对心肌梗死(MI)后大鼠左室重构及心肌细胞凋亡的影响。方法结扎大鼠冠状动脉前降支,随机分成三组:MI组,术后不用药,卡维地洛大剂量组(HCAR组),卡维地洛小剂量组(LCAR组),术后2d分别给予卡维地洛10 mg/kg和1.25 mg/kg。另外不手术不用药组为假手术组(SH组)。6周后测定左室重构指标及心肌细胞凋亡计数。结果卡维地洛用药组与MI组比较,左室重构明显改善,心肌细胞凋亡量明显减少,且有剂量依赖,大剂量组优于小剂量组。结论卡维地洛可改善AMI后大鼠的左室重构,并有剂量依赖性,减少心肌细胞凋亡可能是其重要因素之一。     

卡维地洛、氯沙坦合用防治大鼠心肌梗死左室重构对比

目的对比卡维地洛、氯沙坦及其合用防治大鼠急性心肌梗死(AMI)左室重构(LVRM)的作用.方法雌性SD大鼠分为AMI对照、卡维地洛 (1 mg·kg-1·d-1)、氯沙坦(3 mg·kg-1·d-1)和卡维地洛(1 mg·kg-1·d-1)+氯沙坦(3 mg·kg-1·d-1)组,另设假手术组对照.给药4周后行血流动力学测定和病理分析.结果 AMI各组间梗死面积差异均无显著性(45.8%～46.7%,P值均>0.05).与假手术组相比,AMI组的左室舒张末压(LVEDP)、容积(LVV)、重量(LVW)、室间隔厚度(STh)和右室重量(RVW)均显著增加(P值均<0.01),左室内压最大上升和下降速率(±dp/dp)及其校正值(±dp/dt/LVSP)均显著降低(P值均<0.01).与AMI组相比,卡维地洛、氯沙坦以及合用组的LVEDP、LVV、LVW、STh和RVW均显著降低或减轻(P值均＜0.01),±dp/dt及±dp/dt/LVSP均显著升高(P＜0.05～0.01),且LVEDP和STh在合用组较卡维地洛组降低更显著(P值均<0.01).结论卡维地洛和氯沙坦单用与合用均能有效抑制大鼠AMI后的左室重构,改善血流动力学和左室功能,且以合用更佳.     

卡维地洛防治大鼠急性心肌梗死左室重塑的作用

目的评价第三代β-受体阻滞剂卡维地洛防治大鼠急性心肌梗死(AMI)左室重塑(LVRM)的作用.方法100只雌性SD大鼠AMI术后24h随机分成(1)AMI对照组(n=25);(2) 卡维地洛组(n=25)(1mg·kg-1·d-1);(3)西拉普利组(n=25)(1 mg·kg-1·d-1)和(4)氯沙坦组(n=25)(3mg·kg-1·     

卡维地洛对急性心肌梗塞后晚期心室重构影响的实验研究

目的:观察卡维地洛对大鼠急性心肌梗塞后8周心室重构、血清型胶原氨基末端肽(PNP)水平及左心室功能的影响。方法:结扎雄性大鼠左前降支建立急性心肌梗塞模型,术后24h存活的大鼠16只被随机分为:对照组(n=8)、卡维地洛组(n=8,10mg/kg·d,灌胃给药);另设假手术组(n=8)。术后8周导管法测量血流动力学及左心室功能,形态学测算梗塞面积、左心室扩张指数和球形指数;Masson三色染色测量非梗塞区(NIZ)胶原容积分数(CVF);放免法测量PNP水平。结果:对照组与卡维地洛组大鼠梗塞面积无显著性差异(44.70%vs41.79%)。与假手术组相比,对照组左心室舒张末压(LVEDP),左、右心室相对重量(LVRW、RVRW),室间隔厚度(IVST),左心室扩张指数(LVDI),左心室NIZ的CVF、PNP水平均显著增加(P<0.01~0.001);血压、左心室收缩压(LVSP)、左心室球形指数(LVSI)、左心室内压最大上升和下降速度(±dp/dtmax)及其校正值(±dp/dtmax/LVSP)均显著降低(P<0.01~0.001)。与对照相比,卡维地洛组心率、LVEDP、LVRW、RVRW、IVST、LVDI、非梗塞区CVF、PNP水平显著降低(P<0.01~0.001);LVSI、±dp/dtmax及其校正值(±dp/dtmax/LVSP)显著升高(P<0.01~0.001)。血清PNP含量与LVEDP水平呈显著正相关(r=0.8628,P<0.001)。结论:卡维地洛能有效抑制急性心肌梗塞后左心室非梗塞区胶原增生,减轻大鼠急性心肌梗塞后的左心室重构,改善血流动力学和左心室功能。     

卡维地洛改善急性心肌梗死后左室重构的临床研究

目前研究表明,抑制左室重构的发生是降低急性心肌梗死（acute myocardial infarction,AMI）患者致残及死亡率的关键因素。卡维地洛（carvedilol）通过阻滞肾上腺素β1、β2和α1,受体[1]从而抑制和改善左室重构。     

缬沙坦对急性心肌梗死大鼠左室重构及心功能的影响

目的 研究缬沙坦对大鼠急性心肌梗死（AMI）后左室重构及心功能的影响。方法 将80只雌性SD大鼠AMI后6 h随机分为:梗死对照组（MI-C组,n=30）、缬沙坦治疗组（MI-V组,n=30）及假手术组（Sham组,n=20）。MI-C组及MI-V组结扎冠状动脉左室支建立AMI模型,Sham组只在相同部位穿线后不结扎。MI-V组:将缬沙坦20 mg/(kg·d)以生理盐水15 ml/kg溶解后灌胃,每日2次,共7 d;MI-V组和Sham组:均以等量生理盐水灌胃,每日2次,共7 d。分别于AMI后12 h、3 d 及7 d,测定血流动力学,进行超声和形态学检查。结果 与Sham组比较,MI-C组的左室收缩压（LVSP）、左室内压最大上升速率（+dp/dt）和左室内压最大下降速率（-dp/dt）显著降低（分别为P<0.05及P<0.01）;左室舒张末压（LVEDP）显著增加（P<0.01）;左室舒张末期容积(LVEDV)、短轴(D)、左室相对质量（LVWI）逐渐增加,至7 d时显著增加（P<0.05或P<0.01）;长轴(L)、球形指数、短轴缩短率（FS）逐渐降低,至7 d时显著降低（P<0.05或P<0.01）。与MI-C组比较,MI-V组的LVSP、+dp/dt、-dp/dt显著回升（P<0.05或P<0.01）,LVEDP显著下降（P<0.05或P<0.01）,LVWI逐渐下降,至7 d时降低显著（P<0.05）,梗死范围从3 d、7 d开始显著减小（P<0.05）。LVEDV、D、LVWI及梗死范围均下降,至7 d时显著降低（P<0.05或P<0.01）,L、球形指数、FS逐渐升高,至7 d时显著上升（P<0.05或P<0.01）。结论 缬沙坦能减轻心肌梗死后左室构型的改变,改善早期AMI后大鼠的心功能,抑制左室重构,改善左室的功能。     

超声观察老年急性心肌梗塞后的进行性左室重构

目的观察老年急性心肌梗塞（ＡＭＩ）后进行性左室重构（ＰＬＶＲ）。方法４６例老年ＡＭＩ于入院时、出院前和ＡＭＩ后半年应用Ａｃｕｓｏｎ１２８或ＨＰ１５００型彩色多普勒超声检查。左室舒张末期容量指数（ＥＤＶＩ）每次增长＞８％者归为有ＡＭＩ后ＰＬＶＲ。结果９例有ＡＭＩ后ＰＬＶＲ者较３７例无ＡＭＩ后ＰＬＶＲ者心功能差（Ｐ＜０．０５）。在有ＡＭＩ后ＰＬＶＲ组ＡＭＩ并发症总例数较多（Ｐ＜０．０５）。结论老年人ＡＭＩ病例中心功能差者易发生ＡＭＩ后ＰＬＶＲ。ＡＭＩ并发症与ＡＭＩ后ＰＬＶＲ有关。     

卡维地洛、福辛普利及其合用对急性心肌梗死大鼠左室重塑的影响

本研究通过卡维地洛、福辛普利单剂治疗与联合应用对大鼠急性心肌梗死 (AMI)左室重塑作用的比较探讨二者联合应用对防治AMI左室重塑的影响。1 材料与方法 :取体重 ( 2 2 0± 2 0 )g的Wistar雄性大鼠(第三军医大学动物中心提供 ) ,采用Pfeffer等的手术方法 ,在乙醚麻醉下 ,结扎冠状动脉左前降支 ,同时设立假手术组。术后 2 4h将存活大鼠随机分为 :⑴AMI对照组 (n =10 ) ;⑵卡维地洛组 ( 1mg·kg- 1 ·d- 1 ,n =10 ) ;⑶福辛普利组 ( 10mg·kg- 1 ·d- 1 ,n =10 ) ;⑷二药合用组 (卡维地洛 1mg·kg- 1 ·d- 1 ,福辛普利 10mg·kg- 1 ·d-…     

健心颗粒干预大鼠慢性心力衰竭左室重构的实验研究

目的 探讨健心颗粒干预大鼠慢性心力衰竭（CHF）左室重构的影响。方法 以32周老龄自发性高血压大鼠（SHR）的CHF模型作为研究对象，观察应用健心颗粒4周后的收缩压（SBP）、体重（BW）、左室质量（LVM）、LVM／BW变化，检测血浆血管紧张素Ⅱ（AngⅡ）、心钠素（ANP）、脑钠素（BNP）水平。结果 健心颗粒可以降低SHR的SBP、LVM、LVM／BW，降低血浆AngⅡ、ANP、BNP水平。结论 健心颗粒可以调节神经内分泌细胞因子，减轻左室重构，改善心功能。     

急性心肌梗死后左室重构临床研究

目的　探讨溶栓治疗对急性心肌梗死后左室结构和功能的影响。方法　对 36例首发急性心肌梗死患者于梗死后 4周和 12周进行超声心动图观察。分别测定左室舒张末期容积指数 (LVEDVI)、左室收缩末期容积指数 (LVESVI)、射血分数 (EF) ,作为反映左室结构和功能变化的指标。结果　急性心肌梗死后LVEDVI、LVESVI均明显增高 (分别为P <0 0 1,P <0 0 5 )。 4周和 12周检查发现 ,溶栓组LVEDVI、LVESVI无明显差异 (分别P>0 0 5 ,P >0 0 5 ) ,EF值明显增大 (P <0 0 5 ) ;未溶栓组LVEDVI、LVESVI明显增大 (分别为P <0 0 5 ,P <0 0 5 ) ,EF值无明显变化 (P >0 0 5 ) ;对 4周和 12周的检查结果作组间比较发现 ,溶栓组LVEDVI、LVESVI均小于未溶栓组 (P <0 0 5 ) ,EF值溶栓组高于未溶栓组 (P <0 0 5 )。结论　溶栓治疗能有效地抑制急性心肌梗死后左室重构 ,改善心功能。     

卡维地洛对心梗大鼠远期心室重构的影响及其作用机制

目的:探讨卡维地洛(Carv)对心肌梗死(MI)大鼠心室心肌重构的影响及其作用机制。方法:结扎30只大鼠左冠状动脉建立MI模型后,随机分为Carv组(n=15)及MI组(n=15)。再另设假手术(Sham)组(n=15)。Carv组给予Carv(日剂量2 mg/kg),分2次灌胃;Sham组及MI组均给予等量蒸馏水灌胃。24周后,观察心室重构和左室非梗死区心肌内4-羟基壬烯醛(4-HNE)和过氧化物丙二醛(MDA)的含量及表达。结果:24周后,超声显示,与Sham组比较,MI组大鼠心功能明显降低,左室舒张末期内径(LVEDD)明显增大,左室短轴缩短率(FS)和心脏射血分数(EF)明显降低(P0.05,P0.01)。MI组大鼠左室非梗死区心肌内4-HNE和MDA的含量明显增加,表达明显增强(P0.05,P0.01)。Carv组大鼠左室非梗死区心肌组内4-HNE和MDA的含量比MI组明显降低(P0.05,P0.01)。结论:MI 6月后,心肌内4-HNE、MDA的活性仍然较高,氧化应激反应仍持续,Carv可以促进活性醛的代谢,对心脏具有保护作用,可改善预后。     

Effect of hepatocyte growth factor on left ventricular remodeling after acute myocardial infarction in canine

Background and objectives To investigate the effect of hepatocyte growth factor (HGF) on left ventricular (LV) remodeling after acute myocardial infarction (AMI). Methods AMI was produced by ligation of proximal left anterior descending coronary artery(LAD) in 12 mongrel canines. These animals were randomized into 2 groups. In HGF group (n=6), canines were injected with pcDNA3-HGF lml (about 300ug) at the margin of infarcted myocardium; in control group (n=6) canines were injected with equal volume of normal saline. Cardiac function and left ventricular remodeling were evaluated with echocardiography at 1, 4, 8 weeks after MI. LV myocardium specimens were obtained at 8 weeks and stained with hematoxylin and eosin for histological examination or with sirius red to assess the collagen content. Results Compared with control group, LVEF in HGF group was significantly higher at 4 weeks (49.61+6.66 vs 39.84+6.39; P＜0.05) and at 8 weeks (51.57+8.53 vs 40.61+7.67; P＜0.05) after AMI, while LVESV was significantly lower in HGF group than that in control group at 8 weeks after AMI (18.98+3.47 vs 25.66+5.86; P＜0.05). Posterior left ventricular wall thickness decreased significantly from 1 wk to 8 wks after AMI in control group, while remained unchanged in HGF group. Compared with control group, histological examination showed more neovascularization and less scar, and sirius red staining indicated higher volume of type Ⅲ collagen (7.10&#177;4.06% vs 3.77&#177;1.09%; P＜0.05) and lower collagen Ⅰ/Ⅲ ratio value (1.11&#177;0.52 vs 2.94&#177;2.48; P＜0.05)in HGF group. Conclusion HGF gene transfer might improve cardiac function and LV remodeling after acute myocardial infarction by stimulating angiogenesis, reducing fibrosis, and reducing myocardial scarring.     

EflFect of hepatocyte growth factor on left ventricular remodeling after acute myocardial infarction in canine

Background and objectives To investigate the effect of hepatocyte growth factor (HGF) on left ventricular (LV) remodeling after acute myocardial infarction (AMI). Methods AMI was produced by ligation of proximal left anterior descending coronary artery (LAD) in 12 mongrel canines. These animals were randomized into 2 groups. In HGF group (n=6), canines were injected with pc-DNA3-HGF 1 ml (about 300ug) at the margin of infarcted myocardium; in control group (n=6) canines were injected with equal volume of normal saline. Cardiac function and left ventricular remodeling were evaluated with echocardiography at 1,4, 8 weeks after MI. LV myocardium specimens were obtained at 8 weeks and stained with hematoxylin and eosin for histological examination or with sirius red to assess the collagen content. Results Compared with control group, LVEF in HGF group was significantly higher at 4 weeks (49.61 6.66 vs 39.84 6.39; P<0.05) and at 8 weeks (51.57 8.53 vs 40.61 7.67; P<0.05) after AMI, while LVESV was significantly lower in HGF group than that in control group at 8 weeks after AMI (18.98 3.47 vs 25.66 5.86; P<0.05). Posterior left ventricular wall thickness decreased significantly from 1 wk to 8 wks after AMI in control group, while remained unchanged in HGF group.Compared with control group, histological examination showed more neovascularization and less scar, and sirius red staining indicated higher volume of typeⅢcollagen (7.10±4.06% vs 3.77±1.09%; P<0.05) and lower collagenⅠ/Ⅲratio value (1.11±0.52 vs 2.94±2.48; P<0.05) in HGF group. Conclusion HGF gene transfer might improve cardiac function and LV remodeling after acute myocardial infarction by stimulating angiogenesis, reducing fibrosis, and reducing myocardial scarring.     

肝细胞生长因子对急性心肌梗死后左室重构的预测作用

目的: 探讨血清肝细胞生成因子(HGF)对急性心肌梗死(AMI)后早期左室重构的预测价值。方法: 36例AMI患者入院时及发病7 d测定血清HGF水平;AMI其中的26例分别于发病后7~10 d及发病后3个月行超声心动图检查,3个月时左室舒张末期容积指数（LVEDVI）与7~10 d时比增加≥5 ml/m2定义为左室重构组(n=11),对两组血清HGF值进行比较。结果: AMI患者入院时血清HGF浓度较对照组明显升高［(809±288)ng/L vs.(620±162)ng/L,P<0.01］,7 d时升高更显著［(1 607±1 355)ng/L,P<0.01］。发病7 d时血清HGF浓度在左室重构组较非左室重构组升高［(2 216±1 522)ng/L vs.(1 176±593)ng/L,P<0.05］,而入院时两组浓度则无显著差异。结论: AMI时血清HGF浓度升高,AMI后7 d时增高的血清HGF可能预示心室重构。     

卡维地洛对心肌梗死后左室重塑的影响

目的：观察卡维地洛对急性心肌梗死（AMI）左室重塑的影响。方法：将80例AMI患随机分为常规治疗组（n=20)，依那普利组（n=30)及卡维地洛组（n=30)在AMI后1周，24周用超声心动图分别测定3组病人的左房内径（LA），左室舒张末期内径（LVDd)，左室收缩末期内径（LVDs)，室间膈舒张末期厚度（IVSd)，左室后壁舒张末期厚度（LVPWd)，计算左室重量（LWM），左室重量质数（LVMI）及左室射血分数（LVEF）。结果：AMI后24周，卡维地洛组和依那普利组与常规治疗组比较LA，LVDd,IVDs均明显缩小，IVSd,LVPWd,LVM及LVMI明显减小，而LVEF明显升高（P＜0．01），以上指标卡维地洛组与依那普利组比较无显性差异（P＞0．05），结论：卡维地洛可以防治AMI后左室重塑，改善心功能，其作用与依那普利相同。     

Early mitral regurgitation after acute myocardial infarction does not contribute to subsequent left ventricular remodeling

BACKGROUND: It is well known that mitral regurgitation may lead to left ventricular dilation; however, the relationship between progressive left ventricular dilation after acute myocardial infarction (MI) and mitral regurgitation has not yet been clarified. HYPOTHESIS: This study tested the hypothesis that early mitral regurgitation contributes to left ventricular remodeling after acute MI. METHODS: We prospectively evaluated 131 consecutive patients by serial two-dimensional and Doppler echocardiography on Days 1, 2, 3, and 7, after 3 and 6 weeks, 3 and 6 months, and 1 year following acute MI. Patients were divided into two groups: those with mitral regurgitation in the first week after acute MI (Group 1, n = 34) and those without mitral regurgitation (Group 2, n = 81). RESULTS: Over 1 year, a significant increase in end-diastolic volume index (from 62.1 +/- 12.9 to 70.5 +/- 23.6 ml/m2, p = 0.001) with a strong linear trend (F = 15.1, p < 0.001) was noted. Initial end-diastolic volume index was higher in Group 1 (65.6 +/- 13.3 vs. 60.4 +/- 12.5 ml/m2, p = 0.047), but this difference remained constant throughout the study (F = 1.76, p = NS). Therefore, the pattern of end-diastolic volume changes was similar in both groups during the period of observation. CONCLUSIONS: These data indicate that early mitral regurgitation after acute MI does not contribute to subsequent left ventricular remodeling in the first year after myocardial infarction.     

螺内酯抑制急性前壁心肌梗死患者的左室重构

目的探讨急性前壁心肌梗死患者口服螺内酯对于左室重构的影响。方法将急性前壁心肌梗死患者随机分为两组。对照组30例,接受血管紧张素转换酶抑制剂、β-受体阻滞剂、抗血小板、调脂药物等常规处理。螺内酯组30例,在常规治疗基础上加用螺内酯（40mg,每日1次）。随访1年,并检测脑钠尿肽（BNP）及超声心动图以评价左室功能和左室容积。结果6和12月时螺内酯组血清BNP水平明显低于对照组[（355±74）ng/Lvs（418±77）ng/L,P<0.05和（316±72）ng/Lvs（389±67）ng/L,P<0.05],且12月时螺内酯组较对照组左室舒张末期内径（LVEDD）、左室收缩末期内径（LVESD）明显缩小[LVEDD:（49±6）mmvs（53±5）mm,P<0.05;LVESD:（37±5）mmvs（40±4）mm,P<0.05]。结论螺内酯可抑制急性前壁心肌梗死患者左室重构。     

急性心肌梗死与左室重构

急性心肌梗死(AMI)后左室发生细胞学,分子学及细胞间质的变化,进而引起左室在大小、形态、组织结构和功能状态的改变,此即目前许多研究所提及的AMI后的左室重构.AMI后左室的重构贯穿于整个病程的始终,成为影响AMI患者近远期预后的主要原因之一.