中国基层医药
中國基層醫藥
중국기층의약
CHINESE JOURNAL OF PRIMARY MEDICINE AND PHARMACY
2013年
7期
973-975,后插1
,共4页
唐艳芬%高想%张锋莉%蒋凤荣%姜卫东
唐豔芬%高想%張鋒莉%蔣鳳榮%薑衛東
당염분%고상%장봉리%장봉영%강위동
曲美他嗪%心力衰竭,充血性%心钠素%利钠肽,脑%利钠肽,C型%血管紧张素类%大鼠,Sprague-Dawley
麯美他嗪%心力衰竭,充血性%心鈉素%利鈉肽,腦%利鈉肽,C型%血管緊張素類%大鼠,Sprague-Dawley
곡미타진%심력쇠갈,충혈성%심납소%리납태,뇌%리납태,C형%혈관긴장소류%대서,Sprague-Dawley
Trimetazidine%Heart failure,congestive%Atrial natriuretic factor%Natriuretic peptide,C-type%Natriuretic peptide,brain%Angiotensins%Rats,Sprague-Dawley
目的 探讨盐酸曲美他嗪对慢性心力衰竭(CHF)大鼠模型心功能和神经激素的影响.方法 腹主动脉缩窄法制备SD大鼠心衰模型,心脏超声测定室间隔(IVS)及左室后壁(LVPW)厚度、左室舒张末期内径(LVD)和收缩末期内径(LVS)、左室射血分数(LVEF)和短轴缩短率(FS);观察心肌细胞病理变化;Real-Time PCR定量测定神经激素尿钠肽(BNP)、C型心钠肽受体(NPRC)、心钠肽(ANP)、肌球蛋白重链(β-MHC)、血管紧张素1(AT1);免疫组化测定超氧化物歧化酶(SOD).结果 曲美他嗪高剂量组和模型组比较,IVS、LVPW、LVS、LVD分别为(0.63 ±0.05)mm、(0.73 ±0.06) mm、(0.73±0.05) nn、(0.87±0.06) mm和(1.07 ±0.06)mm、(1.13±0.06)mm、(0.93±0.06) mm、(1.33 ±0.06)mm(P ＜0.05);LVEF、FS分别为(27.75±1.83)％、(11.44±0.76)％和(11.78±0.56)％、(4.27±0.22)％(P＜0.01);心肌细胞结构明显改善;B NP、ANP、NPRC、ATI、β-MHC表达下降,SOD表达升高.结论 曲美他嗪能改善大鼠心衰模型神经激素的分泌,改善心功能.
目的 探討鹽痠麯美他嗪對慢性心力衰竭(CHF)大鼠模型心功能和神經激素的影響.方法 腹主動脈縮窄法製備SD大鼠心衰模型,心髒超聲測定室間隔(IVS)及左室後壁(LVPW)厚度、左室舒張末期內徑(LVD)和收縮末期內徑(LVS)、左室射血分數(LVEF)和短軸縮短率(FS);觀察心肌細胞病理變化;Real-Time PCR定量測定神經激素尿鈉肽(BNP)、C型心鈉肽受體(NPRC)、心鈉肽(ANP)、肌毬蛋白重鏈(β-MHC)、血管緊張素1(AT1);免疫組化測定超氧化物歧化酶(SOD).結果 麯美他嗪高劑量組和模型組比較,IVS、LVPW、LVS、LVD分彆為(0.63 ±0.05)mm、(0.73 ±0.06) mm、(0.73±0.05) nn、(0.87±0.06) mm和(1.07 ±0.06)mm、(1.13±0.06)mm、(0.93±0.06) mm、(1.33 ±0.06)mm(P ＜0.05);LVEF、FS分彆為(27.75±1.83)％、(11.44±0.76)％和(11.78±0.56)％、(4.27±0.22)％(P＜0.01);心肌細胞結構明顯改善;B NP、ANP、NPRC、ATI、β-MHC錶達下降,SOD錶達升高.結論 麯美他嗪能改善大鼠心衰模型神經激素的分泌,改善心功能.
목적 탐토염산곡미타진대만성심력쇠갈(CHF)대서모형심공능화신경격소적영향.방법 복주동맥축착법제비SD대서심쇠모형,심장초성측정실간격(IVS)급좌실후벽(LVPW)후도、좌실서장말기내경(LVD)화수축말기내경(LVS)、좌실사혈분수(LVEF)화단축축단솔(FS);관찰심기세포병리변화;Real-Time PCR정량측정신경격소뇨납태(BNP)、C형심납태수체(NPRC)、심납태(ANP)、기구단백중련(β-MHC)、혈관긴장소1(AT1);면역조화측정초양화물기화매(SOD).결과 곡미타진고제량조화모형조비교,IVS、LVPW、LVS、LVD분별위(0.63 ±0.05)mm、(0.73 ±0.06) mm、(0.73±0.05) nn、(0.87±0.06) mm화(1.07 ±0.06)mm、(1.13±0.06)mm、(0.93±0.06) mm、(1.33 ±0.06)mm(P ＜0.05);LVEF、FS분별위(27.75±1.83)％、(11.44±0.76)％화(11.78±0.56)％、(4.27±0.22)％(P＜0.01);심기세포결구명현개선;B NP、ANP、NPRC、ATI、β-MHC표체하강,SOD표체승고.결론 곡미타진능개선대서심쇠모형신경격소적분비,개선심공능.
Objective To observe the effects of trimetazidine (TMZ) on the cardiac function and neurohormonal of heart failure model in rats.Methods Partially banding abdominal aortic artery to achieve congestive heart failure rats model.Interventricular septum thickness(IVST),left ventricular posterior wall thickness(LVPWT),left ventricular end-diastolic diameter(LVEDD),left ventricular end-systolic diameter (LVESD),left ventricular ejection fraction(LVEF) and shortening fraction(FS) were measured by echocardiogram,Pathological changes of myocardial cells was observed,B-type natriuretic peptide (BNP)、C-type natriuretic peptide receptor (NPRC),atrial natriuretic peptide (ANP),myosin heavy chain (β-MHC) and angiotensinl (AT1) were measured by Real-Time PCR,superoxide dismutase (SOD) was measured by immunohistochemistry method.Results Trimetazidine treatment of the high-dose group and the model group compare IVST LVPWT,LVESD,LVEDD were (0.63 ± 0.05) mn,(0.73 ± 0.06) mm,(0.73 ±0.05)mm,(0.87 ±0.06)mm and (1.07 ±0.06)mm,(1.13 ±0.06) mm,(0.93 ±0.06)mm,(1.33 ±0.06) mm,was significantly reduced (P ＜ 0.05),LVEF,FS increased to (27.75 ± 1.83) ％,(11.44 ± 0.76) ％ and (11.78 ±0.56)％,(4.27 ± 0.22)％ (P ＜ 0.01),Myocardial cell structure were remarkably improved.The expression of BNP,ANP,NPRC,ATI,β-MHC were remarkably decreased.The expression of SOD was elevated.Conclusion TMZ treatment group can improve the secretion of neurohormonal of heart failure model in rats,and also obviously improve the cardiac contractility.
