Electrophysiological changes in rat ventricular myocardium at different stages of experimental diabetes

AIM: To explore the probable mechanisms of diabetes-induced arrhythmias. METHODS: Diabetes was induced in male SD rats, using a single injection of alloxan into tail vein. Untreated age-matched animals were used as controls. All animals were observed by 2, 4, 6 and 8 weeks, respectively. Transmembrane potentials were recorded with conventional glass microelectrodes. RESULTS: Action potential duration(APD) at all level (APD10, APD20, APD30, APD50, APD70, APD90) was significantly lengthened in right ventricular papillary muscle from week 2 of diabetes. At week 8, APD was more lengthened at any level of repolarization than that at week 2. No differences were observed in the maximum rate of depolarization(V_max), overshoot(OS) and action potential amplitude(APA) as well as the resting membrane potential(RP) from the 2th to 8th week of diabetes. CONCLUSION: The results indicate that prolongation of APD may be prominently responsible for the increased incidence of cardiac re-entry-arrhythmias and sudden death, especially at late stages of diabetes.