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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 investigate the protective effect and mechanism of nimodipine on acute myocardial ischemia in rats and its effect on cardiomyocyte apoptosis. Methods: Forty Wistar rats were randomly divided into normal control group, simple ischemic group and nimodipine high and low dose groups, with 10 rats in each group. BL-410 biosignal acquisition system was used to determine the maximal rate of increase / decrease of left ventricular pressure (± dp / dtmax). Cardiomyocyte apoptosis in each group was detected by TUNEL method. Results: (1) Compared with the normal control group, the ± dp / dtmax of the ischemia group was significantly decreased (P <0.01), and the levels of nimodipine in the low and high dose groups were significantly higher than those in the ischemia group (P <0.01) ST segment elevation in myocardial ischemic electrocardiogram was significant after ligation of left anterior descending coronary artery, and ST segment in low and high dose Nimodipine group was lower than that in ischemia group (P <0.01) ; (3) Compared with the normal control group, the number of apoptotic cells in ischemia group increased obviously. Apoptotic cells in nimodipine low and high dose groups decreased significantly, and decreased with dose increasing (P <0.01). Conclusion: Nimodipine can increase the rate of change of left ventricular pressure caused by ischemia and inhibit the apoptosis induced by ischemic injury, thus protecting the myocardium from ischemia.