中国医药
中國醫藥
중국의약
CHINA MEDICINE
2008年
7期
403-406
,共4页
阴祯茜%庄晓峰%李志忠%张京梅
陰禎茜%莊曉峰%李誌忠%張京梅
음정천%장효봉%리지충%장경매
心肌梗死%心室重塑%胶原%卡维地洛
心肌梗死%心室重塑%膠原%卡維地洛
심기경사%심실중소%효원%잡유지락
Myocardial infarction%Ventricle remodeling%Collagen%Carvedilo
目的 卡维地洛对大鼠急性心肌梗死(AMI)后非梗死区胶原重塑的影响.方法 冠状动脉结扎术后24h存活的雌性SD大鼠83只,完全随机分为心肌梗死组43例和卡维地洛组40例.另设假手术组27例;各组按观察时间48h和4周再分为:心肌梗死48h组和心肌梗死4周组,卡维地洛48h组和卡维地洛4周组,假手术48h组和假手术4周组.免疫组织化学方法检测心肌胶元-Ⅰ、胶元-Ⅲ的胶原容积分数(CVF).结果 ①与假手术48h组相比心肌梗死48h组的主动脉收缩压(SBP)、舒张压(DBP)和平均动脉压(MAP)、左心室收缩压(LVSP)和左心室内压最大上升和下降速率(±dp/dt)均降低,差异有统计学意义(P<0.05或P<0.01),左心室舒张末压(LVEDP)则显著升高[(6.06±4.64)对比(1.31±2.67),P<0.05];②与假手术4周组比,心肌梗死4周组仅LVSP、±dp/dt和心率均降低,差异有统计学意义(P<0.05或P<0.01),LVEDP甚至比心肌梗死48 h组更高[(19.86±12.76)对比(6.06±4.64),P<0.01],同时Collagen-Ⅰ、Collagen-Ⅲ的CVF升高,差异有统计学意义(P<0.05);③与心肌梗死48h组相比,卡维地洛48h组的LVSP、±dp/dt和心率均降低,差异有统计学意义(P<0.05或P<0.01),但LVEDP无显著变化,与心肌梗死48h组相比,卡维地洛4周组的LVEDP[(11.93±9.79)对比(19.86±12.76)]、Collagen-Ⅰ、Collagen-Ⅲ的CVF[(3.82.±1.16)对比(8.10±1.77);(2.67±0.82)对比(5.26±1.87)]均降低,差异有统计学意义(P<0.05或P<0.01),但INSP、±dp/dt均无显著变化.结论 AMI后,发生血流动力学和左心室功能异常,非梗死区胶原-I、Ⅲ含量均增加.卡维地洛4周能有效降低AMI后大鼠左心室舒张末压,改善血流动力学和左心功能.卡维地洛治疗对AMI后大鼠非梗死区Ⅰ-型、Ⅲ-型胶原含量的增生有抑制作用.
目的 卡維地洛對大鼠急性心肌梗死(AMI)後非梗死區膠原重塑的影響.方法 冠狀動脈結扎術後24h存活的雌性SD大鼠83隻,完全隨機分為心肌梗死組43例和卡維地洛組40例.另設假手術組27例;各組按觀察時間48h和4週再分為:心肌梗死48h組和心肌梗死4週組,卡維地洛48h組和卡維地洛4週組,假手術48h組和假手術4週組.免疫組織化學方法檢測心肌膠元-Ⅰ、膠元-Ⅲ的膠原容積分數(CVF).結果 ①與假手術48h組相比心肌梗死48h組的主動脈收縮壓(SBP)、舒張壓(DBP)和平均動脈壓(MAP)、左心室收縮壓(LVSP)和左心室內壓最大上升和下降速率(±dp/dt)均降低,差異有統計學意義(P<0.05或P<0.01),左心室舒張末壓(LVEDP)則顯著升高[(6.06±4.64)對比(1.31±2.67),P<0.05];②與假手術4週組比,心肌梗死4週組僅LVSP、±dp/dt和心率均降低,差異有統計學意義(P<0.05或P<0.01),LVEDP甚至比心肌梗死48 h組更高[(19.86±12.76)對比(6.06±4.64),P<0.01],同時Collagen-Ⅰ、Collagen-Ⅲ的CVF升高,差異有統計學意義(P<0.05);③與心肌梗死48h組相比,卡維地洛48h組的LVSP、±dp/dt和心率均降低,差異有統計學意義(P<0.05或P<0.01),但LVEDP無顯著變化,與心肌梗死48h組相比,卡維地洛4週組的LVEDP[(11.93±9.79)對比(19.86±12.76)]、Collagen-Ⅰ、Collagen-Ⅲ的CVF[(3.82.±1.16)對比(8.10±1.77);(2.67±0.82)對比(5.26±1.87)]均降低,差異有統計學意義(P<0.05或P<0.01),但INSP、±dp/dt均無顯著變化.結論 AMI後,髮生血流動力學和左心室功能異常,非梗死區膠原-I、Ⅲ含量均增加.卡維地洛4週能有效降低AMI後大鼠左心室舒張末壓,改善血流動力學和左心功能.卡維地洛治療對AMI後大鼠非梗死區Ⅰ-型、Ⅲ-型膠原含量的增生有抑製作用.
목적 잡유지락대대서급성심기경사(AMI)후비경사구효원중소적영향.방법 관상동맥결찰술후24h존활적자성SD대서83지,완전수궤분위심기경사조43례화잡유지락조40례.령설가수술조27례;각조안관찰시간48h화4주재분위:심기경사48h조화심기경사4주조,잡유지락48h조화잡유지락4주조,가수술48h조화가수술4주조.면역조직화학방법검측심기효원-Ⅰ、효원-Ⅲ적효원용적분수(CVF).결과 ①여가수술48h조상비심기경사48h조적주동맥수축압(SBP)、서장압(DBP)화평균동맥압(MAP)、좌심실수축압(LVSP)화좌심실내압최대상승화하강속솔(±dp/dt)균강저,차이유통계학의의(P<0.05혹P<0.01),좌심실서장말압(LVEDP)칙현저승고[(6.06±4.64)대비(1.31±2.67),P<0.05];②여가수술4주조비,심기경사4주조부LVSP、±dp/dt화심솔균강저,차이유통계학의의(P<0.05혹P<0.01),LVEDP심지비심기경사48 h조경고[(19.86±12.76)대비(6.06±4.64),P<0.01],동시Collagen-Ⅰ、Collagen-Ⅲ적CVF승고,차이유통계학의의(P<0.05);③여심기경사48h조상비,잡유지락48h조적LVSP、±dp/dt화심솔균강저,차이유통계학의의(P<0.05혹P<0.01),단LVEDP무현저변화,여심기경사48h조상비,잡유지락4주조적LVEDP[(11.93±9.79)대비(19.86±12.76)]、Collagen-Ⅰ、Collagen-Ⅲ적CVF[(3.82.±1.16)대비(8.10±1.77);(2.67±0.82)대비(5.26±1.87)]균강저,차이유통계학의의(P<0.05혹P<0.01),단INSP、±dp/dt균무현저변화.결론 AMI후,발생혈류동역학화좌심실공능이상,비경사구효원-I、Ⅲ함량균증가.잡유지락4주능유효강저AMI후대서좌심실서장말압,개선혈류동역학화좌심공능.잡유지락치료대AMI후대서비경사구Ⅰ-형、Ⅲ-형효원함량적증생유억제작용.
Objective To observe the effects of carvedilol on the eollagen remodeling of non-infarction zone in rat model of acute myocardial infarction (AMI). Methods AMI model was established with ligation of anterior descending coronary artery in female SD rats. 24 hours after operation, 83 survivors were randomly divided into AMI control (MI group, n = 43 ), carvedilol [10mg/(kg. d)] treatment (C group, n = 40) group which included a sham-operated group(S group, n = 27). Furthermore, according to observation time, each group was divided into two subgroups: M148 h group, MI4W group; C48h group, C4W group; S48 h group, S4W group. Carvedilol was given to group C by gastric gavage 24h after ligation. The collagen volume fraction (CVF) of type Ⅰ, Ⅲ collagen was detected with immunohistochemistry, in the non-infarction zone (NIZ) of left ventricle. Results Compared with sham-operated 48h group, in MI 48h group, systolic blood pressure (SBP), mean aortic pressure (MAP)、diastolic blood pressure (DBP) and left ventricular systolic pressure (LVSP) and the maximum rate rise of left ventrieular pressure(±dp/dt) significantly decreased (P＜0.05 or P＜0.01), while left ventricular end diastolic pressure(LVEDP) significantly increased(6.06±4.64 vs 1.31±2.67 ,P＜0.05). Compared with sham-operated 4w group, in MI 4w group, only LVSP, ±dp/dt and heart rate significantly decreased (P＜0.05 or P＜0.01), but LVEDP was higher than that of MI48h (19.86±12.76 vs 6.06±4.64 ,P＜0.01). Meanwhile, CVF of type Ⅰ, Ⅲ significantly increased(P＜0.05 or P＜0.01). Compared with MI 48h group, LVSP, ±dp/dt and heart rate significantly decreased in C48h group, but LVEDP did not change. However, compared with MI 4w group, LVEDP(11.93±9.79vs 19.86±12.76) and CVF of type Ⅰ ,Ⅲ(3.82.±1.16vs8.10±1.77;2.67±0.82 vs5.26±1.87 ; respectively) deereased in CAw group (P＜0.05 or P＜0.01), but LVSP and ±dp/dt did not change.Condusion As abnormal hemodynamic and left ventricular function developed after AMI in rats, CVF of type Ⅰ ,Ⅲ increased. 4 weeks' treatment of carvedilol could not only decrease LVEDP, improve left ventrieular function and hemodynamic, but also reduce the increase of CVF of type Ⅰ、Ⅲ in the left ventricle non-infarction zone of rats after AMI.
