Gap junction remodelling is involved in the susceptibility of diabetic rats to hypokalemia-induced ventricular fibrillation.

The objective of the present study was to examine the susceptibility of diabetic rats with cardiomyopathy to hypokalemia-induced ventricular fibrillation and to localize gap junction protein connexin-43 as well as subcellular changes that may be involved in the development of severe arrhythmia. Our results showed a significantly higher incidence of sustained ventricular fibrillation in diabetic hearts as compared with control hearts, 80% vs 20%, respectively. Diabetic cardiomyopathy itself was accompanied by a distinct decrease in connexin-43-immunopositive gap junctions.