摘要
目的探讨血管紧张素Ⅱ受体拮抗剂氯沙坦干预慢性心力衰竭对兔心肌肌浆网钙泵(SERCA2)、钙释放通道(RyR2)、受磷蛋白(PLB)基因表达的影响及意义。方法通过结扎兔冠状动脉前降支复制心肌梗死(心梗)模型,以氯沙坦进行干预。于心梗后8周比较观察左室结构、血流动力学的变化及 SERCA2、RyR2、PLB 基因的表达。结果与对照组相比,心梗组左室舒张末压(LVEDP)显著升高(P<0.01),左室压力上升和下降最大速度(+dp/dt_(max)-dp/dt_(max))显著降低(P<0.01);氯沙坦组 LVEDP 显著低于心梗组(P<0.05),+dp/dt_(max)、-dp/dt_(max)显著高于心梗组(P<0.05)。心梗组 SERCA2、RyR2、PLB mRNA 显著低于对照组(P<0.01),而氯沙坦组的上述三项显著高于心梗组(P<0.05)。结论氯沙坦长期干预心力衰竭,能够改善心脏舒缩功能,可能与其上调肌浆网的钙调控蛋白 SERCA2、RyR2、PLB 的基因表达有关。
Objective To investigate the effects of losartan on mRNA expression of myocardial sarcoplasmic reticulum calcium handling proteins （ SERCA2, RyR2 and PLB） and the role of which in prevention of chronic heart failure in rabbit Methods After chronic heart failure was induced by ligation of the left anterior descending artery in rabbits, the animals were treated with losartan. At 8 weeks after ligation, left ventricular function, hemodynamic parameters, and SERCA2, RyR2, PLB mRNA expressions were observed. Results Compared with the control group （group C）, LVEDP in the infracted group （group Ⅰ ） increased （P 〈 0. 01 ）, while ＋ dp/dtmax and - dp/dtmax decreased significantly （P 〈 0.01 ）. LVEDP was lower but ＋ dp/dtmax and -dp/dtmax significantly higher in the losartan treated group （group L） than those in group （P 〈 0. 05）. SERCA2, RyR2, and PLB mRNA expressions in group I were remarkably lower than those in group L （P 〈 0. 01 ） and group C （P 〈0. 01 ）, respectively. Conclusion Losartan can improve cardiac function, probably owing to its upregulating mRNA expressions of myocardial sarcoplasmic reticulum Ca^2＋ handling proteins （ RyR2, SERCA2 and PLB） in the prevention of heart failure.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
2006年第9期793-796,共4页
Chinese Journal of Cardiology
基金
武汉大学"十五
211工程"重点建设项目经费资助
关键词
氯沙坦
心力衰竭
充血性
钙调蛋白
钙通道
Losartan
Heart failure,congestive
Calmodulin
Calcium channels
