尼莫地平对大鼠急性心肌缺血的保护作用及其对心肌细胞凋亡的影响

The protective effects of nimodiping in acute myocardial ischemia(AMI) injury in rats and its influence on apoptosis of cardiomyocytes

目的:探讨尼莫地平对大鼠急性心肌缺血的保护作用和机制,以及对心肌细胞凋亡的影响。方法:Wistar大鼠40只随机分为正常对照组、单纯缺血组及尼莫地平高、低剂量组,每组10只,采用BL-410生物信号采集系统测定左室内压上升/下降最大速率(±dp/dtmax);用原位末端脱氧核苷酸转移酶标记法(TUNEL法)检测各组心肌细胞凋亡情况。结果:(1)与正常对照组比较单纯缺血组±dp/dtmax显著降低(P<0.01),尼莫地平低、高剂量组明显高于单纯缺血组(P<0.01);(2)结扎左冠状动脉前降支后心肌缺血心电图ST段抬高明显,尼莫地平低、高剂量组ST段均降低,与单纯缺血组相比,差异均有统计学意义(P<0.01);(3)与正常对照组比较,单纯缺血组细胞凋亡数明显增多。尼莫地平低、高剂量组凋亡细胞显著减少,随剂量增加呈递减趋势(P<0.01)。结论:尼莫地平能升高缺血引起的左室内压变化率,抑制缺血损伤引起的细胞凋亡,从而保护缺血对心肌的损伤。

Objective： To explore the protective effects and channel blocker, in acute myocardial ischemia （AMI） injury mechanism of Nimodiping, a kind of calcium in rats and its influence on apoptosis of cardiomyocytes through duplicating the AMI model and the ±dp/dtmax of left ventricular. Methods： Forty Wistar rats were included in the study, divided randomly into 4 groups： normal control group, acute myocardial ischemia group, nimodiping high dose group and nimodiping low dose group. The expression of apoptosis cells were observed by TUNEL immunohistochemical technique. Results： After legating the left anterior descending branch, the ST segment of group c elevated obviously comparing with group d; The ST segment of nimodiping high dose group and group nimodiping low dose group all dropped and the ECG data have a statistical significance compared with the acute myocardial ischemia group separately; Nimodiping could depress human AMI apoptosis. The expression of apoptosis increased significantly as compared with that in group normal control group （P 〈0.01）. Conclusion： Nimodiping can protect myocardium from AMIR injury by inhibiting the apoptosis of cardiomyocytes induced by Nimodiping