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目的探讨β受体阻滞剂卡维地洛干预慢性心衰对心肌肌浆网(sarcoplasmic reticulum,SR)Ca2+泵活性和Ca2+释放通道(Type 2 Ryanodine receptor,RyR2)密度的影响及意义。方法通过结扎大鼠左冠脉建立慢性心衰模型,以大剂量卡维地洛(60mg·kg-1·d-1)进行干预,对照观察血流动力学、左室心肌SRCa2+泵活性、[3H]-ryanodine与RyR2最大结合量(Bmax)及Kd值。结果与假手术组(SH组)相比,心衰组(HF组)左室舒张末压(LVEDP)显著升高(P<0.01),左室压力上升、下降最大速度(+dp/dtmax、-dp/dtmax)显著降低(P<0.01),卡维地洛(Carv组)LVEDP显著低于心衰组(P<0.01),+dp/dtmax、-dp/dtmax显著高于心衰组(P<0.01);心衰组心肌SRCa2+泵活性、[3H]-ryanodine与RyR2最大结合量Bmax显著低于假手术组(P<0.01),卡维地洛组显著高于心衰组(P<0.01),3组Kd值差异不显著(P>0.05)。结论大剂量卡维地洛长期干预心梗后慢性心衰,能够改善心肌SRCa2+泵活性,增加RyR2密度,并改善心肌舒缩功能。
Objective To investigate the effect and significance of β-blocker carvedilol on chronic heart failure on pump Ca2 + pump activity and type 2 Ryanodine receptor (RyR2) density in cardiac sarcoplasmic reticulum (SR). Methods Chronic heart failure model was established by ligation of the left coronary artery in rats. High-dose carvedilol (60 mg · kg-1 · d-1) was used for intervention. The hemodynamics, SRCa2 + pump activity, 3H] -ryanodine and RyR2 maximum binding capacity (Bmax) and Kd value. Results Compared with SH group, left ventricular end-diastolic pressure (LVEDP) and left ventricular ejection fraction (LVEDP) in HF group were significantly increased (P <0.01) (P <0.01). LVEDP in carvedilol group was significantly lower than that in heart failure group (P <0.01), and dp / dtmax and -dp / dtmax were significantly higher than those in heart failure group (P <0.01). The myocardial SRCa2 + pump activity and the maximum binding capacity of [3H] -ryanodine and RyR2 in heart failure group were significantly lower than those in sham-operation group and carvedilol group (P < 0.01). There was no significant difference in Kd between three groups (P> 0.05). Conclusion Long-term intervention of high-dose carvedilol for chronic heart failure after myocardial infarction can improve myocardial SRCa2 + pump activity, increase RyR2 density, and improve myocardial contractility.