腹主动脉缩窄术不同结扎位置致慢性心力衰竭大鼠模型比较
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摘要
目的:比较腹主动脉缩窄术不同结扎位置致慢性心力衰竭(CHF)大鼠模型的病理及病理生理特点。方法:将45只健康成年雄性SD大鼠随机分为3组:近心结扎组(A组,n=15只)、远心结扎组(B组,n=15只)、正常对照组(C组,n=10只)。A、B组行不同部位腹主动脉缩窄术,C组仅分离出腹主动脉后挂线标记不结扎。建模8周后行超声心动图评价心功能指标,检测血清脑利钠肽(BNP)水平,计算心肌质量指数,观察心肌组织病理学变化。结果:建模8周后,A、B、C组的存活率分别为60%、80%、100%,组间比较差异无统计学意义(P>0.05);与C组比较,A、B组均表现为不同程度皮毛松弛,光泽度降低,精神萎靡,进食量及活动量下降,呼吸频率加快等CHF症状,且A组症状更明显;A、B组心脏舒张末期左心室后壁厚度(LVP-Wd)、左心室重量指数(LVW/BW)值、心脏重量指数(HWI)值及血清脑利钠肽(BNP)水平明显高于C组(P<0.05),且A组高于B组(P<0.01);A、B组左心室射血分数(LVEF)、左心室短轴缩短率(LVFS)及体重(BW)均低于C组(均P<0.05),且A组低于B组(P<0.01);A组心肌细胞肥大,肌纤维结构排列紊乱,大量小血管增生,心肌细胞间隙有大量炎性细胞浸润及胶原纤维明显增多;B组心肌细胞肥大,肌纤维结构排列紊乱,小血管壁增厚,心肌细胞间隙有少量炎性细胞及胶原纤维;C组心肌细胞大小正常,排列整齐,心肌形态结构未见异常。结论:近心端结扎腹主动脉缩窄术致CHF症状及程度更明显,更接近其病理生理进展过程,可优先选择该方法建立CHF模型。
Objective:To compare the pathologic and pathophysiologic characteristics of two experimental models of chronic heart failure(CHF)establishted by different ligation sites of abdominal aortic constriction.Methods:SD rats were randomized to subject either proximal cardiac ligation(group A,n=15)or telecentric ligation(group B,n=15)to induce CHF models.A total of 10 rats without ligation were selected as normal controls(group C).The cardiac function indicators were detected by echocardiography.The serum brain natriuretic peptide(BNP)level was measured.The myocardial mass index was calculated.Myocardial histopathological changes were observed after 8 weeks of modeling.Results:At 8 weeks post-operation,the survival rate in groups A,B and C was 60%,80%and 100%.respectively.Compared with group C,the rats in group A and B exhibited CHF symptoms including loose fur,low gloss,low mental retardation,decreased food intake and activity,and increased respiratory rate,etc.The left ventricular mass index(LVW/BW),cardiac weight index(HWI)and serum BNP content in group A and B were significantly higher than those in group C,while the left ventricular ejection fraction(LVEF),left ventricular short axis shortening rate(LVFS)and body weight(BW)were notably lower(P<0.05).The changes in group A were more obvious.The histopathological changes in group A showed hypertrophic cardiomyocytes,muscle fiber structure arranged disorder,thickened small vessel walls,increased inflammatory cells and collagen fibers in the space of cardiomyocytes.The histopathological changes of group B were similar to those of group A except for a small number of inflammatory cells and collagen fibers.In the contrary,normal size of cardiomyocytes,neatly arranged myocardial cells,and normal morphologic structure of myocardium were observed in group C.Conclusion:Proximal cardiac ligation of abdominal aortic was effective in inducing CHF,which might be more appropriate for establishing CHF model.
Objective:To compare the pathologic and pathophysiologic characteristics of two experimental models of chronic heart failure(CHF)establishted by different ligation sites of abdominal aortic constriction.Methods:SD rats were randomized to subject either proximal cardiac ligation(group A,n=15)or telecentric ligation(group B,n=15)to induce CHF models.A total of 10 rats without ligation were selected as normal controls(group C).The cardiac function indicators were detected by echocardiography.The serum brain natriuretic peptide(BNP)level was measured.The myocardial mass index was calculated.Myocardial histopathological changes were observed after 8 weeks of modeling.Results:At 8 weeks post-operation,the survival rate in groups A,B and C was 60%,80%and 100%.respectively.Compared with group C,the rats in group A and B exhibited CHF symptoms including loose fur,low gloss,low mental retardation,decreased food intake and activity,and increased respiratory rate,etc.The left ventricular mass index(LVW/BW),cardiac weight index(HWI)and serum BNP content in group A and B were significantly higher than those in group C,while the left ventricular ejection fraction(LVEF),left ventricular short axis shortening rate(LVFS)and body weight(BW)were notably lower(P<0.05).The changes in group A were more obvious.The histopathological changes in group A showed hypertrophic cardiomyocytes,muscle fiber structure arranged disorder,thickened small vessel walls,increased inflammatory cells and collagen fibers in the space of cardiomyocytes.The histopathological changes of group B were similar to those of group A except for a small number of inflammatory cells and collagen fibers.In the contrary,normal size of cardiomyocytes,neatly arranged myocardial cells,and normal morphologic structure of myocardium were observed in group C.Conclusion:Proximal cardiac ligation of abdominal aortic was effective in inducing CHF,which might be more appropriate for establishing CHF model.
引文
[1]VOLTERRANI M,IELLAMO F.Cardiac rehabilitation in patients with heart failure:new perspectives in exercise training[J].Card Fail Rev,2016,2(1):63.
[2]WEINHEIMER C J,LAI L,KELLY D P,et al.Novel mouse model of left ventricular pressure overload and infarction causing predictable ventricular remodelling and progression to heart failure[J].Clin Exp Pharmacol Physiol,2015,42(1):33-40.
[3]伍凤仪,朱林强,张银霞,等.腹主动脉缩窄术致心力衰竭大鼠模型肾脏损伤的探究[J].现代医院,2016,16(12):1735-1737.
[4]ALLA J A,GRAEMER M,FU X,et al.Inhibition of G-protein-coupled receptor kinase 2prevents the dysfunctional cardiac substrate metabolism in fatty acid synthase transgenic mice[J].J Biol Chem,2016,291(6):2583-2600.
[5]TANNENBAUM S,SAYER G T.Advances in the pathophysiology and treatment of heart failure with preserved ejection fraction[J].Curr Opin Cardiol,2015,30(3):250.
[6]ZHAO C Z,ZHAO X M,YANG J,et al.Inhibition of farnesyl pyrophosphate synthase improves pressure overload induced chronic cardiac remodeling[J].Sci Rep,2016(6):39186.
[7]芦玲巧,曾翔俊,郝刚.大鼠心力衰竭模型的构建与鉴定[J].中国比较医学杂志,2012,22(8):22-25.
[8]SEYMOUR A M L,GILES L,BALL V,et al.In vivo assessment of cardiac metabolism and function in the abdominal aortic banding model of compensated cardiac hypertrophy[J].Cardiovasc Res,2015,106(2):249-260.
[9]POLSINELLI V B,SINHA A,SHAH S J.Visceral congestion in heart failure:right ventricular dysfunction,splanchnic hemodynamics,and the intestinal microenvironment[J].Curr Heart Fail Rep,2017,14(6):519-528.
[10]SALVADOR A M,NEVERS T,VELAZQUEZ F,et al.Intercellular adhesion molecule 1regulates left ventricular leukocyte infiltration,cardiac remodeling,and function in pressure overload-induced heart failure[J].J Am Heart Assoc,2016,5(3):e003126.
[11]韦超料,江波,武志锋.N端脑利钠肽前体与慢性心力衰竭患者心功能分级和早期预后的关系[J].广西医学,2015,44(5):680-682.
[2]WEINHEIMER C J,LAI L,KELLY D P,et al.Novel mouse model of left ventricular pressure overload and infarction causing predictable ventricular remodelling and progression to heart failure[J].Clin Exp Pharmacol Physiol,2015,42(1):33-40.
[3]伍凤仪,朱林强,张银霞,等.腹主动脉缩窄术致心力衰竭大鼠模型肾脏损伤的探究[J].现代医院,2016,16(12):1735-1737.
[4]ALLA J A,GRAEMER M,FU X,et al.Inhibition of G-protein-coupled receptor kinase 2prevents the dysfunctional cardiac substrate metabolism in fatty acid synthase transgenic mice[J].J Biol Chem,2016,291(6):2583-2600.
[5]TANNENBAUM S,SAYER G T.Advances in the pathophysiology and treatment of heart failure with preserved ejection fraction[J].Curr Opin Cardiol,2015,30(3):250.
[6]ZHAO C Z,ZHAO X M,YANG J,et al.Inhibition of farnesyl pyrophosphate synthase improves pressure overload induced chronic cardiac remodeling[J].Sci Rep,2016(6):39186.
[7]芦玲巧,曾翔俊,郝刚.大鼠心力衰竭模型的构建与鉴定[J].中国比较医学杂志,2012,22(8):22-25.
[8]SEYMOUR A M L,GILES L,BALL V,et al.In vivo assessment of cardiac metabolism and function in the abdominal aortic banding model of compensated cardiac hypertrophy[J].Cardiovasc Res,2015,106(2):249-260.
[9]POLSINELLI V B,SINHA A,SHAH S J.Visceral congestion in heart failure:right ventricular dysfunction,splanchnic hemodynamics,and the intestinal microenvironment[J].Curr Heart Fail Rep,2017,14(6):519-528.
[10]SALVADOR A M,NEVERS T,VELAZQUEZ F,et al.Intercellular adhesion molecule 1regulates left ventricular leukocyte infiltration,cardiac remodeling,and function in pressure overload-induced heart failure[J].J Am Heart Assoc,2016,5(3):e003126.
[11]韦超料,江波,武志锋.N端脑利钠肽前体与慢性心力衰竭患者心功能分级和早期预后的关系[J].广西医学,2015,44(5):680-682.