摘要
目的 观察阿霉素诱导心肌病时细胞凋亡关键酶caspase-3活性与超声心动图、脑利钠肽（BNP）的动态变化关系.方法 雄性Wistar大鼠60只,尾静脉注射阿霉素2.5 mg/kg,每周1次,连续注射10周.于末次注射停药后观察2周.在0、2、4、6、8、10、12周各时间点测量血清BNP水平、超声心动图和caspase-3活性;12周末测定血流动力学、全心质量指数（HW/BW）,HE染色观察其组织学变化.结果 与对照组相比,阿霉素组BNP水平升高;左室射血分数（LVEF）、左室短轴缩短率（LVFS）、左室收缩压（LVSP）、左室舒张末压（LVDP）、左室最大压力上升及下降速度（±dp/dtmax）均明显降低;Caspase-3活性与基础值、对照组相比明显升高.相关性分析Caspase-3与LVEF、LVFS呈负相关（r=-0.9368,P=0.0.018;r=-0.9222,P=0.003）;Caspase-3与BNP呈正相关（r=0.8937,P=0.0410）.结论 小剂量长疗程使用阿霉素能引起心肌细胞的凋亡,最终造成大鼠心脏结构和功能的改变.可早期利用超声心动图测定LVFS、LVEF和BNP来检测早期阿霉素所致的心脏结构和功能改变.
Objective To observe the relationship of Caspase-3 activity, echocardiography and BNP on adriamycin-induced cardiomyopathy. Methods 60 male wistar rats, tail vein injection of adriamycin 2.5 mg/kg week, continuous injection of 10 weeks. The end of the injection was observed 2 weeks after drug withdrawal. Serum BNP levels, echocardiography and Caspase-3 activity were measured at 0, 2, 4, 6, 8, 10 and 12 weeks. Hemodynamics, whole-hearted mass/body mass index were measured at 12 weekends. The histological changes were observed by HE staining. Results Compared with the control group, levels of BNP elevated on adriamycin group. Left ventricular ejection fraction （LVEF）, fractional shortening （LVFS）, left ventrieular systolic pressure （LVSP）, left ventricular end-diastolic pressure （LVDP）, left ventrlcular maximum rate of pressure rise and fall （~dp/dt~） were decreased, Caspase-3 activity and the basis of value, significantly higher than the control group. Caspase-3 were negative correlation with LVEF, LVFS （r=-0.9368, P=0.0181, r=-0.9222, P=0.0031）. Cas- pase-3 and BNP were positively correlated （r=0.8937, P=0.0410）. Conclusion Small dose and long treatment courses of Adriamycin can cause apoptosis of myocardial cells and ultimately result in cardiac structure and func- tion in rats changes. Early use of eehocardiography can be measured fractional shortening, ejection fraction and BNP to detect the early stage of adriamycin-induced changes in cardiac structure and function.
出处
《中国心血管病研究》
CAS
2010年第5期380-383,共4页
Chinese Journal of Cardiovascular Research
