Ischaemic preconditioning reduced the incidence of ventricular fibrillation during a subsequent 25-minute occlusion from 40% to 0% (p<0.05) and increased survival from 0% to 40%.
Does ischaemic preconditioning reduce ischaemia and reperfusion-induced arrhythmias in a canine model of prolonged coronary occlusion, and is this mediated by cyclo-oxygenase products?
Ischaemic preconditioning protects against arrhythmias and improves survival during prolonged coronary occlusion in a canine model, an effect that appears to be mediated by the cyclo-oxygenase pathway.
Absolute Event Rate: 0% vs 40%
p-value: p=<0.05
STUDY OBJECTIVE: The aim was to determine whether short (preconditioning) occlusions of a coronary artery protect against the arrhythmias occurring during a subsequent more prolonged occlusion and to examine whether the observed protection is mediated by the release of a product of the cyclo-oxygenase pathway of arachidonic acid metabolism. DESIGN: The effects were examined of two short (5 min) coronary artery occlusions, in chloralose-urethane anaesthetised dogs, on a subsequent prolonged (25 min) occlusion; analysis of ischaemia and reperfusion induced arrhythmias and of epicardial ST segment changes was performed. EXPERIMENTAL MATERIAL: 46 anaesthetised mongrel dogs in a restricted body weight range were used. MEASUREMENTS AND MAIN RESULTS: Preconditioning reduced the incidence and severity of ischaemic arrhythmias during a 25 min occlusion. Ventricular premature beats (VPB) reduced from 445 (SEM 140) to 96(22) (p less than 0.01), ventricular fibrillation (VF) from 4/10 to 0/20 (p less than 0.05), and ventricular tachycardia from 9/10 to 6/20 (p less than 0.05). VF following reperfusion was reduced from 6/6 to 6/10 (p less than 0.05). Preconditioning thus increased survival from the prolonged ischaemia-reperfusion insult from 0% to 40%. The protective effect of preconditioning was lost in the presence of the cyclo-oxygenase inhibitor sodium meclofenamate (2 mg.kg-1), eg, VPBs 367(95), VF during occlusion 1/9 and during reperfusion 8/8, survival 0%. CONCLUSIONS: Short, preconditioning periods of myocardial ischaemia protect the myocardium against the arrhythmogenic effects of a more prolonged occlusion. That this protection is lost if the cyclo-oxygenase pathway is blocked suggests a protective role for prostanoids, most likely prostacyclin, as endogenous myocardial protective substances.
Végh et al. (Sat,) conducted a other in Myocardial ischaemia and arrhythmias (n=46). Ischaemic preconditioning vs. No preconditioning was evaluated on Ventricular fibrillation during a 25-minute occlusion (p=<0.05). Ischaemic preconditioning reduced the incidence of ventricular fibrillation during a subsequent 25-minute occlusion from 40% to 0% (p<0.05) and increased survival from 0% to 40%.