Objective: 

It has been reported that blockade of IKATP current exerts a protective effect against arrhythmias in ischemic myocardium. Nevertheless, authors suggest that the opening of this channel protects ischemic myocardium. We have investigated the effect of glibenclamide, an IKATP blocker, on electrophysiological stability by analyzing the signal regularity of induced ventricular fibrillation (VF), in isolated hearts subjected to regional ischemia.

Methods: 

Eighteen NZW rabbits were anaesthetized (ketamine, 10 mg/kg i.v.), killed and the hearts excised, isolated and perfused in a Langendorff system. A pacing electrode and a plaque with 256 recording electrodes were positioned on the left ventricle. VF was induced by pacing, maintaining the perfusion. The dominant frequency of VF was obtained by a spectral analysis. The spectrum concentration (percentage of the total power spectrum, contained in a range of ± 1 hertz around the dominant frequency) as an index of the signal regularity was determined. Five minutes after VF induction, the circumflex coronary artery occlusion (CAO) was performed. Measurements were obtained before and five minutes after CAO. Glibenclamide (10 mM) was infused (treated group), through the aortic root.

A two-factor ANOVA with repeated measures on one factor was used for comparisons.

Results: 

Spectral concentration (SC) decreased (p<0,05) after CAO, in control (18 ± 3% vs. 24 ± 5%; n=9) but not in treated group. SC was higher (p<0,05) in treated than control group after CAO (25 ± 4% vs. 18 ± 3%; n=9).

Conclusions: 

KATP channel blockade prevents against fibrillatory signal deterioration due to ischemia. This observation reinforces the idea that the blockade of this channel has a beneficial electrophysiological effect.

Acknowledgement: 

This research was supported by a grant (DEP2010-22318-C02-01) from the Ministerio de Ciencia e Innovacion, Spain.