An increase in spatial dispersion of ventricular refractory periods reflects inhomogeneity of ventricular refractoriness and is associated with an increased risk of life-threatening ventricular arrhythmias. Spatial dispersion in ventricular refractoriness is determined by the differences in refractory periods of myocytes in epicardium, midmyocardium and endocardium. Prolongation of ventricular repolarisation with drugs or physical means may reduce the spatial dispersion and the risk of arrhythmia. An increase in coronary flow has been shown to prolong the duration of ventricular repolarisation measured from epicardium in the intact animal heart. We hypothesised that an increase in coronary flow may also prolong ventricular repolarisation cross the three layers of ventricular myocardium through the release of nitric oxide. The simultaneously prolongation of transmural repolarisation may reduce the spatial dispersion of ventricular repolarisation and hence, the risk of life-threatening ventricular arrhythmias.