ABSTRACT
Objective To investigate the alterations and molecular mechanism of transient outward potassi- um currents(I_(to)) in ventricular myocytes from diabetic rats and explore the mechanism of predisposition of arrhyth- mias in diabetes.Methods The diabetes model was established by a single injection of streptozocin(STZ,65 mg/ kg,pH=4.5) I.P.in male Sprague-Dawley rats with weight 150-200 g.Ventricular myocytes were isolated by enzymatic perfusion.The currents were recorded with the whole-cell patch clamp technique,and gene expres- sions of channel-forming subunits (Kv4.2,Kv4.3 and Kv1.4) were semi-quantified by the technique of reverse transcriptase-polymerase chain reaction(RT-PCR).Results The I_(to) density (+70 mV) decreased significantly in diabetic rats compared with controls[control:(30.6?3.8)pA/pF(n=9) vs diabetes:(18.9?3.3)pA/pF(n= 29)(P