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目的探讨曲美他嗪(TMZ)对慢性心衰家兔心肌能量代谢的影响及其保护作用。方法新西兰兔30只,随机分为4组:假手术组(n=6),手术组(n=8):结扎腹主动脉复制心衰模型,手术给药组1(TMZ,n=8),手术给药组2(卡托普利,n=8),分别于术后第4天口服给药。实验8周后,观察TMZ对家兔慢性心衰时心脏血流动力学各项指标(HR、LVSP、LVEDP、±dp/dt_(max))及心肌高能磷酸盐(ATP、PCr)代谢的影响,同时比较血浆心钠素水平、心质量指数的变化。结果(1)与假手术组相比,手术组发生不同程度的心衰症状,表现为心脏收缩功能的减退,心肌肥厚,血浆心钠素水平显著升高,同时心肌高能磷酸盐含量显著减少(均P<0.01)。(2)手术给药组(TMZ、卡托普利)的血流动力学各项指标明显优于手术组,且心肌肥厚明显减轻,血浆心钠素水平明显下降,心肌高能磷酸盐含量明显增加(均P<0.05),给药组组间比较差异无统计学意义(P>0.05)。结论TMZ可显著改善慢性心衰心脏的心功能,减轻心肌肥厚,其作用机制可能与增加心衰心肌内的高能磷酸盐储备有关。
Objective To investigate the effect of trimetazidine on myocardial energy metabolism in rabbits with chronic heart failure and its protective effect. Methods Thirty New Zealand rabbits were randomly divided into 4 groups: sham operation group (n = 6), operation group (n = 8): abdominal aorta replication heart failure model, , Surgery group 2 (captopril, n = 8), were orally administered on the 4th day after surgery. After 8 weeks of experiment, the effects of TMZ on cardiac hemodynamics (HR, LVSP, LVEDP, ± dp / dt max) and myocardial ATP metabolism in chronic heart failure rabbits , While comparing plasma atrial natriuretic peptide levels, cardiac mass index changes. Results (1) Compared with the sham-operation group, the operation group had different degrees of heart failure symptoms, which showed the decrease of systolic function, hypertrophy of myocardium, plasma atrial natriuretic peptide level and significant decrease of high-energy phosphate content in myocardium All P <0.01). (2) The indexes of hemodynamics in TMZ and captopril group were significantly better than those in operation group, and the myocardial hypertrophy was significantly reduced, the level of plasma atrial natriuretic peptide was significantly decreased and the content of high-energy phosphate in myocardium was significantly increased (All P <0.05), there was no significant difference between the two groups (P> 0.05). Conclusion TMZ can significantly improve cardiac function and reduce cardiac hypertrophy in patients with chronic heart failure, and its mechanism may be related to the increase of high-energy phosphate reserves in myocardial tissue of heart failure.