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In order to investigate the role of KATPchannel activation and repolarization dispersion on the ‘border zone’ arrhythmias induced by ischaemia‐reperfusion, the effects of glibenclamide and bimakalim, agents modifying action potential (AP) duration, were studied in an in vitromodel of myocardial ‘border zone’.The electrophysiological effects of 10 μMglibenclamide and 1 μMbimakalim (n=8 each), respectively KATPchannel blocker and activator, were investigated on guinea‐pig ventricular strips submitted partly to normal conditions (normal zone, NZ) and partly to simulated ischaemic then reperfused conditions (altered zone, AZ).By preventing the ischaemia‐induced AP shortening (P<0.0001), glibenclamide reduced the dispersion of AP duration 90% (APD90) between NZ and AZ (P<0.0001), and concomitantly inhibited the ‘border zone’ arrhythmias induced by an extrastimulus (ES), their absence being significantly related to the lessened APD90dispersion (χ2=8.28, P<0.01).Bimakalim, which also reduced the APD90dispersion (P<0.005) due to differential AP shortening in normal and ischaemic tissues, decreased the incidence of myocardial conduction blocks (25% of preparations versus 83% in control, n=12, P<0.05) and favoured ‘border zone’ spontaneous arrhythmias (75% of preparations versus 25% in control, P<0.05).During reperfusion, unlike bimakalim, glibenclamide inhibited the ES‐induced arrhythmias and reduced the incidence of the spontaneous ones (12% of preparations versus 92% in control, P<0.05), this latter effect being significantly related (χ2=6.13, P<0.02) to the lessened ischaemia‐induced AP shortening in the presence of glibenclamide (P<0.0001).These results suggest that KATPblockade may protect the ischaemic‐reperfused myocardium from ‘border zone’ arrhythmias concomitantly with a reduction of APD90dispersion between normal and ischaemic regions. Conversely, KATPchannel activation may modify the incidence of conduction blocks and exacerbate the ischaemia‐induced ‘border zone’ arrhythmias.