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Altered gene expression may underlie prolonged duration of the QT interval and ventricular action potential in streptozotocin-induced diabetic rat heart

机译:基因表达改变可能是链脲佐菌素诱发的糖尿病大鼠心脏QT间期延长和心室动作电位的基础

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Ventricular electrical conduction has been investigated in the streptozotocin (STZ)-induced diabetic rat. Diabetes was induced with a single injection of STZ (60 mg/kg bodyweight, ip). The ECG was measured continuously, in vivo, using a biotelemetry system. Left ventricular action potentials were recorded with an extracellular suction electrode. Expression of mRNA transcripts for selected ion transport proteins was measured in left ventricle with real-time RT-PCR. At 10 weeks after STZ treatment, in vivo heart rate (HR) was reduced (267 ± 3 vs. 329 ± 5 BPM), QRS complex duration and QT interval were prolonged in diabetic rats compared to controls. In vitro spontaneous HR was reduced and paced heart action potential repolarization was prolonged in diabetic rats compared to controls. The mRNA expression for Kcnd2 (I to channel) and Kcne2 (I kr channel) was significantly reduced in diabetic rats compared to controls. Altered gene expression and, in particular, genes that encode K+ channel proteins may underlie delayed propagation of electrical activity in the ventricular myocardium of STZ-induced diabetic rat.
机译:在链脲佐菌素(STZ)诱导的糖尿病大鼠中已经研究了心室电传导。单次注射STZ(60 mg / kg体重,腹腔注射)可诱发糖尿病。使用生物遥测系统在体内连续测量ECG。用细胞外吸引电极记录左心室动作电位。通过实时RT-PCR在左心室中测量所选离子转运蛋白的mRNA转录表达。与对照组相比,STZ治疗后10周,体内心率(HR)降低(267±3 vs. 329±5 BPM),QRS复合体持续时间和QT间隔延长。与对照组相比,糖尿病大鼠的体外自发性HR降低,心脏搏动的起搏电位复极时间延长。与对照组相比,糖尿病大鼠中Kcnd2(I to 通道)和Kcne2(I kr 通道)的mRNA表达显着降低。基因表达的改变,尤其是编码K + 通道蛋白的基因可能是STZ诱导的糖尿病大鼠心室心肌电活动延迟传播的基础。

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