大鼠急性心肌缺血损伤后心脏结构和功能改变的超声心动图评价
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摘要
目的对大鼠急性心肌缺血损伤后心脏结构和功能改变进行超声心动图评价。方法 30只雄性大鼠随机分为假手术组,模型组,地尔硫卓组,每组10只。采用冠状动脉左前降支结扎的方法建立大鼠急性心肌缺血损伤模型。模型建立后连续给药15 d后,采用心脏超声检测左心室结构的功能的改变,包括左心室射血分数(EF),左心室短轴缩短率(FS),每搏输出量(SV),心输出量(CO),左心室舒张末期和收缩末期内径(LVIDd和LVIDs),舒张末期和收缩末期左心室后壁厚度(LVPWd和LVPWs),舒张末期和收缩末期左室前壁厚度(LVAWd和LVAWs)等指标;采用伊文思蓝和TTC染色法测定左心室扩张程度;采用ELISA方法检测血清氨基末端脑钠肽前体(NT-proBNP)水平;并在光镜下观察各组心肌组织HE染色的病理改变。结果心脏超声显示,与假手术组比较,模型组大鼠LVIDd和LVIDs明显增加,而LVAWd、LVAWs、LVPWd和LVPWs明显降低(P<0.05或P<0.01);同时血清NT-proBNP水平升高,左心室腔明显扩张。与模型组比较,地尔硫卓能够明显降低大鼠心肌缺血后LVIDd和LVIDs,增加LVAWd,LVAWs,LVPWd和LVPWs;同时血清NT-proBNP水平下降,抑制左心室腔扩大(P<0.05或P<0.01)。结论心脏超声多种指标结合能够很好地评价大鼠急性心肌缺血损伤后心脏结构和功能改变,将成为小动物心血管疾病研究的主要手段。
Objective To evaluate cardiac structure and function in rats with acute ischemic myocardial injury by ultrasound cardiogram. Methods SD rats were randomly divided into three groups: sham group, model group with ischemic myocardial injury, and a diltiazem treatment group(10 mg/kg). Myocardial ischemic injury was induced by ligating the left anterior descending coronary artery. Left ventricular structure and function were measured by ultrasound cardiogram after 15 d. The parameters included EF, FS, SV, CO, LVIDd, LVIDs, LVPWd, LVPWs, LVAWd and LVAWs were assessed. The serum concentration of NT-proBNP was assessed using ELISA. Left ventricular dilation was analyzed through Evans and TTC staining. HE staining was used for the pathological examination of myocardial structure. Results Compared with the sham group, the degree of left ventricular dilation, the serum levels of NT-proBNP, and LVIDd and LVIDs were significantly decreased in the model group, but LVPWd, LVPWs, LVAWd and LVAWs were increased. Diltiazem treatment decreased LVIDd and LVIDs, and increased LVAWd, LVAWs, LVPWd, and LVPWs, compared with the model group, as assessed using an ultrasound cardiogram analysis. The diltiazem group also showed a significant decrease in serum NT-proBNP levels, and left ventricular dilation compared with the model group. Conclusions An ultrasound cardiogram analysis is suitable as the primary method for evaluating cardiac structure and function in small laboratory animals with angiocardiopathies.
Objective To evaluate cardiac structure and function in rats with acute ischemic myocardial injury by ultrasound cardiogram. Methods SD rats were randomly divided into three groups: sham group, model group with ischemic myocardial injury, and a diltiazem treatment group(10 mg/kg). Myocardial ischemic injury was induced by ligating the left anterior descending coronary artery. Left ventricular structure and function were measured by ultrasound cardiogram after 15 d. The parameters included EF, FS, SV, CO, LVIDd, LVIDs, LVPWd, LVPWs, LVAWd and LVAWs were assessed. The serum concentration of NT-proBNP was assessed using ELISA. Left ventricular dilation was analyzed through Evans and TTC staining. HE staining was used for the pathological examination of myocardial structure. Results Compared with the sham group, the degree of left ventricular dilation, the serum levels of NT-proBNP, and LVIDd and LVIDs were significantly decreased in the model group, but LVPWd, LVPWs, LVAWd and LVAWs were increased. Diltiazem treatment decreased LVIDd and LVIDs, and increased LVAWd, LVAWs, LVPWd, and LVPWs, compared with the model group, as assessed using an ultrasound cardiogram analysis. The diltiazem group also showed a significant decrease in serum NT-proBNP levels, and left ventricular dilation compared with the model group. Conclusions An ultrasound cardiogram analysis is suitable as the primary method for evaluating cardiac structure and function in small laboratory animals with angiocardiopathies.
引文
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[14] Madamanchi C,Alhosaini H,Sumida A,et al.Obesity and natriuretic peptides,BNP and NT-proBNP:mechanisms and diagnostic implications for heart failure[J].Int J Cardiol,2014,176(3):611-617.
[15] Tomiyama H,Nishikimi T,Matsumoto C,et al.Longitudinal changes in late systolic cardiac load and serum NT-proBNP levels in healthy middle-aged Japanese men[J].Am J Hypertens,2015,28(4):452-458.
[16] Xu Y,Yang Y,Luo YQ.Effect of atorvastatin on serum oxidative stress and N-terminal brain natriuretic peptide expression in rats[J].Asian Pac J Trop Med,2014,7(5):398-401.
[17] Drexler H,Depenbusch JW,Truog AG,et al.Effects of diltiazem on cardiac function and regional blood flow at rest and during exercise in a conscious rat preparation of chronic heart failure (myocardial infarction) [J].Circulation,1985,71(6):1262-1270.
[2] Pistner A,Belmonte S,Coulthard T,et al.Murine echocardiography and ultrasound imaging[J].J Vis Exp,2010(42):1-4.
[3] 李粮辉,陈文华,郑宏.改进的TTC染色法显示大鼠心肌缺血再灌注损伤[J].中国实验动物学报,2014,22(5):75-78.
[4] Rat Genome Sequencing Project Consortium.Genome sequence of the Brown Norway rat yields insights into mammalian evolution[J].Nature,2004,428(6982):493-521.
[5] Hou Y,Huang C,Cai X,et al.Improvements in the establishment of a rat myocardial infarction mode[J].J Int Med Res,2011,39(4):1284-1292.
[6] Tanaka M,Richard VJ,Murry CE,et al.Superoxide dismutase plus catalase therapy delays neither cell death nor the loss of the TTC reaction in experimental myocardial infarction in dogs[J].J Mol Cell Cardiol,1993,25(4):367-378.
[7] Zhao XY,Hu SJ,Li J,et al.rAAV-asPLB transfer attenuates abnormal sarcoplasmic reticulum Ca2+ -ATPase activity and cardiac dysfunction in rats with myocardial infarction[J].Eur J Heart Fail,2008,10(1):47-54.
[8] Colazzo F,Castiglioni L,Sironi L,et al.Murine left atrium and left atrial appendage structure and function:echocardiographic and morphologic evaluation[J].PLoS One,2015,10(4):e0125541.
[9] Xu Q,Ming Z,Dart AM,et al.Optimizing dosage of ketamine and xylazine in murine echocardiography[J].Clin Exp Pharmacol Physiol,2007,34(5-6):499-507.
[10] Biala A,Tauriainen E,Siltanen A,et al.Resveratrol induces mitochondrial biogenesis and ameliorates Ang II-induced cardiac remodeling in transgenic rats harboring human renin and angiotensinogen genes[J].Blood Press,2010,19(3):196-205.
[11] Yasuda N,Akazawa H,Ito K,et al.Agonist-independent constitutive activity of angiotensin II receptor promotes cardiac remodeling in mice[J].Hypertension,2012,59(3):627-633.
[12] Wang J,Zhou J,Ding X,et al.Qiliqiangxin improves cardiac function and attenuates cardiac remodeling in rats with experimental myocardial infarction[J].Int J Clin Exp Pathol,2015,8(6):6596-6606.
[13] Cheng H,Lu M,Hou C,et al.Relation between N-terminal pro-brain natriuretic peptide and cardiac remodeling and function assessed by cardiovascular magnetic resonance imaging in patients with arrhythmogenic right ventricular cardiomyopathy[J].Am J Cardiol,2015,115(3):341-347.
[14] Madamanchi C,Alhosaini H,Sumida A,et al.Obesity and natriuretic peptides,BNP and NT-proBNP:mechanisms and diagnostic implications for heart failure[J].Int J Cardiol,2014,176(3):611-617.
[15] Tomiyama H,Nishikimi T,Matsumoto C,et al.Longitudinal changes in late systolic cardiac load and serum NT-proBNP levels in healthy middle-aged Japanese men[J].Am J Hypertens,2015,28(4):452-458.
[16] Xu Y,Yang Y,Luo YQ.Effect of atorvastatin on serum oxidative stress and N-terminal brain natriuretic peptide expression in rats[J].Asian Pac J Trop Med,2014,7(5):398-401.
[17] Drexler H,Depenbusch JW,Truog AG,et al.Effects of diltiazem on cardiac function and regional blood flow at rest and during exercise in a conscious rat preparation of chronic heart failure (myocardial infarction) [J].Circulation,1985,71(6):1262-1270.
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