Glibenclamide, but not class III drugs, prevents ischaemic shortening of the refractory period in guinea-pig hearts.

The effective refractory period was measured in paced (4 Hz) perfused guinea-pig hearts in vitro. The effective refractory period was linearly correlated with temperature of the perfusing solution: as temperature was reduced the effective refractory period was increased. Reduction of the coronary flow rate to 10% of control resulted in a marked reduction in the effective refractory period. UK-66,914, dofetilide, ibutilide and phentolamine caused a prolongation in the effective refractory period, but during ischaemia the effective refractory period was reduced by the same degree as in vehicle-treated hearts. Glibenclamide had no effect on the effective refractory period prior to ischemia but it abolished the ischaemia-induced shortening. These results suggest that the opening of KATP channels may be responsible for the ischaemia-induced shortening of the effective refractory period in perfused guinea-pig hearts and that the class III effects of UK-66,914, dofetilide and ibutilide are attenuated during ischaemia.