RESUMEN
Objective To determine the effect of calmodulin-dependent kinase Ⅱ (CaMK Ⅱ ) -ryanodinereceptor pathway signaling in rabbits with left ventricular bypertrophy (LVH) and triggered ventricular arrhythmia.Methods Forty New Zealand rabbits were randomized into four groups ( n =10 per group):the sham operation group,LVH group,KN-93 (CaMKⅡ inhibitor) group (LVH + KN-93),and the ryanodinegroup ( LVH + ryanodine).Rabbits in the LVH,KN-93,and ryanodinegroups were used to establish a left ventricular hypertrophy model by the coarctation of the abdominal aorta,while the rabbits in the sham operation group did not have the coarctation.After eight weeks,action potentials (APs) were recorded simultaneously in the endocardium and epicardium,and transmural electrocardiogram (ECG) was also recorded in the wedge shaped models of rabbits' left ventricular myocardium.Drugs were administered to animals in the KN-93 and ryanodinegroups respectively,and the frequency of triggered APs and ventricular tachycardia were recorded after isoprenaline ( 1 μmol/L),and high-frequency electrical stimulation were given to rabbits.Results The incidences (animals/group) of triggered APs were:sham,0/10 ; LVH,10/10; KN-93,4/10; and ryanodine,1/10.The incidences of ventricular tachycardia induced were 0/10,9/10,3/10,and 1/10,respectively.The incidences of triggered ventricular arrhythmias in the KN-93 group and ryanodine groups tachycardia or ventricular fibrillation were 0/10,7/10,2/10,and 1/10,respectively.The incidences of triggered ventricular arrhythmias in the KN-93 group and ryanodine groups were much lower than that in the LVH group (P ＜ 0.05).Conclusions KN-93 and ryanodinecan effectively reduce the occurrence of triggered ventricular arrhythmia in rabbits with LVH.The CaMK Ⅱ-ryanodine signaling pathway can be used as a novel target site of treating ventricular arrhythmia.