乐卡地平对心肌梗死大鼠心肌重构的影响(英文)

目的 :观察乐卡地平对心肌梗死大鼠心肌重构的影响。方法 :雄性Wistar大鼠 ,结扎冠状动脉左前降支 ,造成心肌梗死。实验分为 4组 :假手术组、心肌梗死模型组、卡托普利组、乐卡地平组。在结扎冠状动脉后 3h开始 ,分别灌胃给予生理盐水、生理盐水、卡托普利 5 0mg·kg- 1和乐卡地平 2 .5mg·kg- 1,qd ,共 35d。给药容积均为 10mL·kg- 1。最后一次给药后 2 4h ,处死大鼠取心脏 ,测定全心重量和体重比 (THW /BW )、梗死范围 (IS)、左心室内径 (LVD)、室间隔厚度 (ST) ,用天狼猩红染色 ,在图像分析系统下测量心肌间质胶原容积系数 (ICVF)和血管周围胶原容积系数 (PCVF)。结果 :心肌梗死模型组大鼠的THW /BW (0 .38±s 0 .0 3) % ]和LVD (8.8± 1.4 )mm ]均显著比假手术组(0 .32 5± 0 .0 16 ) % ;(6 .5± 0 .3)mm ]大 (P <0 .0 5 ,P <0 .0 1) ,ST(1.71± 0 .2 2 )mm ]则明显比假手术组 (2 .75± 0 .18)mm ]小 (P <0 .0 1) ,IS为(2 6± 3) %。与模型组比较 ,卡托普利和乐卡地平组大鼠的IS(18± 6 ) % ,(19± 7) % ]和LVD(7.5±0 .8)mm ,(7.7± 0 .9)mm]显著变小 (P <0 .0 5 ,P <0 .0 1) ;ST(2 .4± 0 .4 )mm ,(2 .4± 0 .5 )mm]显著变大 (P <0 .0 5 ,P <0 .0 1)。心肌梗死模型组大鼠心肌ICVF和PCVF?

Effect of lercanidipine on myocardial remodeling induced by myocardial infarction in rats

AIM: To observe the effect of lercanidipine on myocardial remodeling induced by myocardial infarction (MI). METHODS: MI was induced by permanent ligation of the left anterior descending coronary artery (LAD) in male Wistar rats. Rats were randomly divided into four groups: sham operation group, MI model group, captopril 50 mg*kg-1 group and lercanidipine 2.5 mg*kg-1 group. Three hours after the operation, the drugs or normal saline were administrated ig qd for 35 d. Twenty four hours after the last administration, rats were sacrificed and hearts were harvested. The ratio of total heart weight to body weight (THW/BW), infarct size (IS), septal thickness (ST) and left ventricular diameter (LVD) were measured. Myocardial interstitial collagen volume fraction (ICVF) and perivascular collagen volume fraction (PCVF) were shown with picrosirius red stain (the collagen specific) and measured by image analysis system. RESULTS: THW/BW, LVD and ST of sham operation group were (0.325±s 0.016) %, (6.5±0.3)mm and (2.75±0.18)mm, respectively. In MI model group, with an IS of (26±3) %, THW/BW ((0.38±0.03) %) and LVD ((8.8±1.4)mm) were significantly increased (P<0.05, P<0.01), and ST((1.71±0.22)mm) decreased (P<0.01), compared with those in sham operation group. In captopril or lercanidipine group, IS ((18±6) %, (19±7) %) and LVD ((7.5±0.8)mm, (7.7±0.9)mm) were significantly smaller than those in MI model group(P<0.05, P<0.01), and ST ((2.4±0.4)mm, (2.4±0.5)mm) was significantly larger than that in MI model group (P<0.01). The ICVF and PCVF of the myocardium in the MI model group ((6.7±1.0) %, (67.41±0.11) %) were significantly larger than those in sham operation group ((4.0±0.5) %; (43.40±0.11) %, P<0.01 or P<0.05). In the captopril and lercanidipine groups, ICVF of myocardium was (5.0±1.0) % and (4.913±0.012) %, respectively, which was significantly smaller than that in MI model group (P<0.01). The PCVF of myocardium in the captopril and lercanidipine groups ((47.54±0.15) %, (46.18±0.18) %) were significantly decreased (P<0.01), compared with that in MI model group. CONCLUSION: Lercanidipine can improve myocardial remodeling induced by myocardial infarction in the rat.