卡托普利对慢性压力负荷性心力衰竭大鼠心肌细胞凋亡的影响

Effects of captopril on rate of cardiomyocyte apoptosis in rats with cardiac failure induced by chronic pressure overload

目的探讨卡托普利对慢性压力负荷性心力衰竭（心衰）大鼠心肌细胞凋亡的影响。方法选择90只SD大鼠，按随机数字表法分为假手术组、模型组、卡托普利组。采用腹主动脉缩窄法复制慢性压力负荷性心衰大鼠模型，分别于药物干预6周（每组10只）、10周时（3组分别存活11、12、13只）应用流式细胞仪测定各组大鼠心肌细胞凋亡率。结果假手术组和模型组10周时细胞凋亡率与6周时比较差异均无统计学意义（均P〉0．05），卡托普利组10周时较6周明显降低[（4．79±0．61）％比（6．80±0．89）％，P〈0．01]；模型组、卡托普利组药物干预6周、10周时心肌细胞凋亡率均明显升高，与假手术组同期比较差异均有统计学意义[6周：（10．08±0．95）％、（6．80±0．89）％比（2．45±0．44）％，10周：（10．60±0．65）％、（4．79±0．61）％比（2．62±0．45）％，均P〈O．01]；卡托普利组心肌细胞凋亡率明显下降，与模型组同期比较差异均有统计学意义（均P〈0．01）。结论卡托普利能减少心肌细胞的凋亡，从而改善充血眭心衰大鼠的心脏功能。

Objective To test the effects of captopril on cardiomyocyte apoptosis in rats with chronic pressure overloaded heart failure. Methods A total of 90 Sprague-Dawley （SD） rats were randomly divided into three groups ： sham operation group, model group and captopril treatment group. The models of rats were established by constricting the abdominal aorta partly. The rate of cardiomyocyte apoptosis in each group was respectively measured by flow cytometry 6 weeks （each, n=10） and 10 weeks （n=11, 12, 13 in the three groups, respectively） after medicine intervention. Results In either the sham operation group or the model group, the rates of cardiomyocyte apoptosis at the time points of 6 and 10 weeks had no statistically significant difference from each other （both P〉 0.05）. However, the rate of captopril treatment group was decreased obviously in 10 weeks compared with that in 6 weeks [ （4.79±0.61）% vs. （6.80±0.89）%, P〈0.01]. The cardiomyocte apoptosis rates in model and eaptopril treatment groups were markedly increased compared with those at the same time in the sham operation group （6 weeks ： （10.08±0.95） %, （6.80±0.89） % vs. （2.45±0.44） % ; 10 weeks ： （10.60±0.65） %, （439±0.61） % vs. （2.62±0.45） %, all P〈0.013. The rates of apoptosis in captopril treatment group were declined sharply compared with those at the same time in the model group in 6 weeks and 10 weeks （both P〈0.01）. Conclusion Captopril can decrease the cardiomyocyte apoptosis and improve the myocardial function in rats with congestive heart failure.