中国老年学杂志
中國老年學雜誌
중국노년학잡지
CHINESE JOURNAL OF GERONTOLOGY
2010年
3期
350-352
,共3页
魏群%杨杰%赵东明%宋显晶%杨萍
魏群%楊傑%趙東明%宋顯晶%楊萍
위군%양걸%조동명%송현정%양평
雷米普利%大鼠%心衰%血管紧张素Ⅱ-受体1
雷米普利%大鼠%心衰%血管緊張素Ⅱ-受體1
뢰미보리%대서%심쇠%혈관긴장소Ⅱ-수체1
Ramipril%Rats%Heart failure%AT1-receptor
目的 研究心肌梗死后心衰大鼠非梗死区心肌血管紧张素Ⅱ(Ang Ⅱ)及其Ⅰ型受体(AT1-R)表达对心室重构的影响及雷米普利的干预作用.方法 结扎大鼠左冠状动脉前降支并饲养6 w的16只存活大鼠,随机分为模型组及雷米普利组,每组8只,另取8只大鼠为假手术组,连续灌胃给药4 w后测定大鼠血流动力学参数,ELISA方法检测血清及左心室非梗死区AngⅡ的含量,RT-PCR 法测定左心室非梗死区心肌组织AT1-R mRNA表达水平,Masson染色观察非梗死区心肌胶原的沉积.结果 雷米普利能明显升高左心室内压最大上升和最大下降速率(±dp/dt_(max)),降低左心室收缩压(LVSP)、左心室舒张末压(LVEDP)(P<0.05或P<0.01),但对心率(HR)、收缩压(SBP)、舒张压(DBP)无明显影响(P>0.05),同时明显降低血清及左心室非梗死区AngⅡ的含量及下调AT1-R mRNA 表达水平(P<0.01或P<0.001),Masson染色可见非梗死区心肌胶原沉积明显减轻.结论 雷米普利对梗死后心衰大鼠非梗死区心肌间质胶原重构有显著的抑制作用,其作用机制与下调AT1-R表达水平及减轻胶原沉积有关.
目的 研究心肌梗死後心衰大鼠非梗死區心肌血管緊張素Ⅱ(Ang Ⅱ)及其Ⅰ型受體(AT1-R)錶達對心室重構的影響及雷米普利的榦預作用.方法 結扎大鼠左冠狀動脈前降支併飼養6 w的16隻存活大鼠,隨機分為模型組及雷米普利組,每組8隻,另取8隻大鼠為假手術組,連續灌胃給藥4 w後測定大鼠血流動力學參數,ELISA方法檢測血清及左心室非梗死區AngⅡ的含量,RT-PCR 法測定左心室非梗死區心肌組織AT1-R mRNA錶達水平,Masson染色觀察非梗死區心肌膠原的沉積.結果 雷米普利能明顯升高左心室內壓最大上升和最大下降速率(±dp/dt_(max)),降低左心室收縮壓(LVSP)、左心室舒張末壓(LVEDP)(P<0.05或P<0.01),但對心率(HR)、收縮壓(SBP)、舒張壓(DBP)無明顯影響(P>0.05),同時明顯降低血清及左心室非梗死區AngⅡ的含量及下調AT1-R mRNA 錶達水平(P<0.01或P<0.001),Masson染色可見非梗死區心肌膠原沉積明顯減輕.結論 雷米普利對梗死後心衰大鼠非梗死區心肌間質膠原重構有顯著的抑製作用,其作用機製與下調AT1-R錶達水平及減輕膠原沉積有關.
목적 연구심기경사후심쇠대서비경사구심기혈관긴장소Ⅱ(Ang Ⅱ)급기Ⅰ형수체(AT1-R)표체대심실중구적영향급뢰미보리적간예작용.방법 결찰대서좌관상동맥전강지병사양6 w적16지존활대서,수궤분위모형조급뢰미보리조,매조8지,령취8지대서위가수술조,련속관위급약4 w후측정대서혈류동역학삼수,ELISA방법검측혈청급좌심실비경사구AngⅡ적함량,RT-PCR 법측정좌심실비경사구심기조직AT1-R mRNA표체수평,Masson염색관찰비경사구심기효원적침적.결과 뢰미보리능명현승고좌심실내압최대상승화최대하강속솔(±dp/dt_(max)),강저좌심실수축압(LVSP)、좌심실서장말압(LVEDP)(P<0.05혹P<0.01),단대심솔(HR)、수축압(SBP)、서장압(DBP)무명현영향(P>0.05),동시명현강저혈청급좌심실비경사구AngⅡ적함량급하조AT1-R mRNA 표체수평(P<0.01혹P<0.001),Masson염색가견비경사구심기효원침적명현감경.결론 뢰미보리대경사후심쇠대서비경사구심기간질효원중구유현저적억제작용,기작용궤제여하조AT1-R표체수평급감경효원침적유관.
Objective To investigate the effects of Ramipril on the content of angiotensin Ⅱand the expression of AT1-R mRNA in heart failure rats after acute myocardial infarction (AMI) in noninfarction zone(NIZ).Methods The rat models of heart failure were established by left anterior descending coronary artery deligation. After 6 w, 24 surviving rats were divided into sham,model and Ramipril groups at random,8 rats in each,and were treated with medicines by intragastric administration respectively. At 10 w, left ventricular end-diastolic pressure (LVEDP), left ventricular systolic pressure(LVSP), +dp/dtmax and-dp/ dtmaxof left ventricular pressure were measured. In addition, the contents of Ang Ⅱ in serum and in non-infarction zone were quantified with ELISA, the expression of AT1-R mRNA was detected by RT-PCR in NIZ. Furthermore, myocardial pathological changes were observed by light microscope after Masson dyeing. Results Ramipril decreased significantly LVSP and LVEDP, the contents of AngⅡ in serum and in non-infarction zone, downregulated AT1-R mRNA expression in NIZ(P<0.05~0.01),whereas increased ±dp/dtmax(P<0.05~0.01), lightened collagen deposition in NIZ with Masson dyeing, but no influence on HR, SBP and DBP(P>0.05). Conclusions Ramipril inhibit myocardial interstitial collagen reconstitution on heart failure after AMI, which may be related to downregulating AT1-R mRNA expression and lightening collagen deposition in NIZ in the development heart failure.