Abstract
Purpose: It has been proposed that chronic exercise produces a KATP channel blockade in ischemic myocardium. We have also reported that channel blockade and training exert very similar effects on energy required to defibrillate. In fact it is postulated that one mechanism by which exercise exerts an antiarrhythmic effect, is by blocking KATP channel. We have analyzed the evolution of spectrum characteristics of ventricular fibrillation (VF), in normoxic conditions and after acute myocardial ischemia, in isolated hearts from trained rabbits, and in hearts submitted to KATP channel blockade. Our hypothesis is that the spectrum characteristics of VF evolve similarly in trained hearts and in hearts undergoing KATP channel blockade. Material and method: 12 NZW rabbits were submitted to a six-week endurance exercise training program, and 14 rabbits (glibenclamide group) and 17 rabbits (control group) were not trained. After exercise program, rabbits were anaesthetized (ketamine, 10 mg/kg i.v.), euthanized 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. The blockade of KATP channels was performed by glibenclamide (10 μM). VF was induced at increasing frequencies. Five minutes after VF triggering, the circumflex coronary artery was occluded. Dominant frequency (DF) of VF was determined by a spectral analysis. Determinations were analyzed 5min after the onset of VF and 60 and 180 s after coronary occlusion. An ANOVA test (two factors) repeated on one factor was used to comparisons. Differences were significant when p<0.05. Results: See Table. View this table: Dominant frequency of VF Conclusions: Unlike what occurs with other parameters, the effect of training on the evolution of VF characteristics in the ischemic myocardium does not appear to be mediated by the blockade of KATP channel.
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