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目的 探讨慢性心衰心肌肌浆网 (SR)Ca2 + 释放通道 (RyR2 )数量及其mRNA表达的变化及ACEI干预的影响及意义。方法 通过结扎大鼠左冠脉建立慢性心衰模型 ,以培哚普利进行干预 ,对照观察血流动力学、[3 H]-ryanodine与左室心肌RyR2 最大结合量 (Bmax)和Kd 值、RyR2 mRNA表达水平。结果 与对照组 (C组 )相比 ,心衰组 (F组 )LVEDP显著升高 (P <0 .0 1) ,+dp/dtmax、-dp/dtmax显著降低 (P <0 .0 1) ,培哚普利组 (P组 )LVEDP显著低于F组 (P <0 .0 1) ,+dp/dtmax、-dp/dtmax显著高于F组 (P<0 .0 1)。F组 [3 H]-ryanodine与RyR2 最大结合量Bmax显著低于C组 (P <0 .0 1) ,P组显著高于F组 (P <0 .0 1) ,三组Kd 值无显著差异 (P >0 .0 5 ) ;F组RyR2 mRNA表达水平显著低于C组 (P <0 .0 1) ,P组显著高于F组 (P <0 .0 1)。结论 慢性心衰心肌SRCa2 + 释放通道数量及其mRNA表达水平降低 ,培哚普利长期干预慢性心衰 ,能够增加RyR2 基因表达 ,增加RyR2 数量 ,可能与其改善心肌收缩功能有关
Objective To investigate the changes of myocardial Ca2 + release channel (RyR2) and its mRNA expression in chronic heart failure (CHF) and the effect and significance of ACEI intervention. Methods Chronic heart failure model was established by ligation of left coronary artery in rats. Perindopril intervention was used to observe the hemodynamics, Bmax and Kd of [3 H] -ryanodine and RyR2 in left ventricular myocardium, RyR2 mRNA expression level. Results Compared with the control group (C group), the LVEDP, FDP and dtmax were significantly lower in group F (P <0.01) LVEDP in perindopril group (P group) was significantly lower than that in F group (P <0.01), and dp / dtmax and -dp / dtmax in perindopril group were significantly higher than those in F group (P <0.01). The maximal binding capacity of [3 H] -ryanodine to RyR2 in group F was significantly lower than that in group C (P <0.01), that in group P was significantly higher than that in group F (P <0.01) (P> 0.05). The mRNA expression of RyR2 in group F was significantly lower than that in group C (P <0.01). The level of RyR2 mRNA in group F was significantly higher than that of group F (P <0.01). Conclusions The number of SRCa2 + releasing channels and their mRNA expression in chronic heart failure are decreased. Perindopril can prolong chronic heart failure, increase RyR2 gene expression and increase RyR2, which may be related to the improvement of myocardial contractile function