国际医药卫生导报
國際醫藥衛生導報
국제의약위생도보
INTERNATIONAL MEDICINE & HEALTH GUIDANCE NEWS
2009年
21期
24-27
,共4页
氨氯地平%CHF%ET-1%BNP
氨氯地平%CHF%ET-1%BNP
안록지평%CHF%ET-1%BNP
Amlodipine%CHF%ET-1%BNP
目的 探讨氨氯地平对充血性心力衰竭(CHF)大鼠血浆中内皮素-1(ET-1)和B型钠尿肽(BNP)表达的影响.方法 SD大鼠随机分为3组:对照组、心衰组、氨氯地平组.CHF组大鼠腹腔注射阿霉素累积剂量达20mg/kgBW制作CHF模型,氨氯地平组大鼠腹腔注射阿霉素同时每天给予氨氯地平10mg/kg.4周后各组大鼠经颈内动脉插管至左心室行血流动力学测定,同时测定大鼠血浆中ET-1和BNP的含量.结果 CHF组大鼠左室压力最大上升速率(+dp/dtmax)和最大下降速率(-dp/atmax)均显著低于对照组,其血浆内ET-1和BNP均显著高于对照组(P<0.01).氨氯地平组±dp/dtmax均显著低于对照组但高于CHF组,其血浆内ET-1和BNP均显著高于对照组低于CHF组(P<0.01).结论 氨氯地平治疗CHF大鼠的作用机制之一可能是通过保护CHF大鼠左室功能、结构及心肌细胞,间接降低ET-1、BNP表达水平.
目的 探討氨氯地平對充血性心力衰竭(CHF)大鼠血漿中內皮素-1(ET-1)和B型鈉尿肽(BNP)錶達的影響.方法 SD大鼠隨機分為3組:對照組、心衰組、氨氯地平組.CHF組大鼠腹腔註射阿黴素纍積劑量達20mg/kgBW製作CHF模型,氨氯地平組大鼠腹腔註射阿黴素同時每天給予氨氯地平10mg/kg.4週後各組大鼠經頸內動脈插管至左心室行血流動力學測定,同時測定大鼠血漿中ET-1和BNP的含量.結果 CHF組大鼠左室壓力最大上升速率(+dp/dtmax)和最大下降速率(-dp/atmax)均顯著低于對照組,其血漿內ET-1和BNP均顯著高于對照組(P<0.01).氨氯地平組±dp/dtmax均顯著低于對照組但高于CHF組,其血漿內ET-1和BNP均顯著高于對照組低于CHF組(P<0.01).結論 氨氯地平治療CHF大鼠的作用機製之一可能是通過保護CHF大鼠左室功能、結構及心肌細胞,間接降低ET-1、BNP錶達水平.
목적 탐토안록지평대충혈성심력쇠갈(CHF)대서혈장중내피소-1(ET-1)화B형납뇨태(BNP)표체적영향.방법 SD대서수궤분위3조:대조조、심쇠조、안록지평조.CHF조대서복강주사아매소루적제량체20mg/kgBW제작CHF모형,안록지평조대서복강주사아매소동시매천급여안록지평10mg/kg.4주후각조대서경경내동맥삽관지좌심실행혈류동역학측정,동시측정대서혈장중ET-1화BNP적함량.결과 CHF조대서좌실압력최대상승속솔(+dp/dtmax)화최대하강속솔(-dp/atmax)균현저저우대조조,기혈장내ET-1화BNP균현저고우대조조(P<0.01).안록지평조±dp/dtmax균현저저우대조조단고우CHF조,기혈장내ET-1화BNP균현저고우대조조저우CHF조(P<0.01).결론 안록지평치료CHF대서적작용궤제지일가능시통과보호CHF대서좌실공능、결구급심기세포,간접강저ET-1、BNP표체수평.
Objective To explore the effect of amlodipine on the expression of ET-1 and BNP in plasma of rats with congestive heart failure.Methods Rats were diveded into three groups,control,chronic heart failure and amlodipine therapy group.Chronic heart failure was induced with adriamycin 20 mg·kg-1 BW.Rats in amlodipine group received amlodipine 10 mg ·kg-1·d-1 and adriamycin at the same time.Hemodynamic measurement was carried out after 4 weeks and the contents of ET-1 and BNP in plasma of each group were detected.Results Compared with control group,the ±dp/dtmax in chronic heart failure group significantly decreased,and the expression of ET-1 and BNP in plasma significantly increased(P<0.01).The ± dp/dtmax in amlodipine group was significantly lower than that in control but obviously higher than that in chronic heart failure group,and the expression of ET-1 and BNP in plasma was significantly higher than that in control but obviously lower than that in chronic heart failure group(P<0.01).Conclusions One mechanism of amlodipine treatment of rats with congestive heart failure may be indirectly reduced the expression of ET-1 and BNP through maintaining the function and structure of left ventricular and protecting cardiac cells.
