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.

Objective To investigate the protective effect of ischemic preconditioning (IPC) and penehyclidine hydrochloride (PHC) on the spinal cord against ischemia-reperfusion injury induced by aortic cross-clamping in rabbits. Methods Twenty-four rabbits were randomly divided into sham operation group (A), ischemia-reperfusion injury group (B) and IPC+PHC group (C). In group C, IPC was performed for 5 min, followed by reperfusion for 30 min, and PHC (0.2 mg/kg) was given at 20 min of rcperfusion. Then, in group B and C, the infrarenal aorta was clamped for 40 min followed by 7 d reperfusion. The aorta was not clamped in group A. The plasma concentrations of malondialdehede (MDA), superoxide dismutase (SOD), creatine kinase (CK) and creatine kinase BB isoenzyme (CK-BB) were assayed at 10 min before clamping, before unclamping, at 60 min and on the 7 th day after unclamping. After an operation, the neurological outcomes of the hind limbs were evaluated, the morphology of the spinal cord was observed, and the apoptotic spinal cord cells were measured by immunohistochemical technique. Results The concentrations of MDA, CK and CK-BB after ischemia-reperfusion in group B were increased significantly compared with those before clamping and　those in group A (P<0.05 or 0.01); the concentrations in group C were higher than those before clamping　(P<0.05), but lower significantly than those in group B (P<0.01), and not significantly different from　those in group A. SOD was opposite. The apoptotic cells in group B were much more than that in groupA and in group C, but the number in group C was significantly higher than that in group A (P<0.01). The incidence rate of paralysis in group C was significantly lower than that in group B, and the neurological score of hinder limb was higher in group C than in group B (P<0.01). Pathological changes of the spinal cord was milder in group C than in group B. Conclusion The combination of IPC and PHC can protect the spinal cord from ischemia-reperfusion injury in rabbits; the main mechanism may be increasing antioxidant potential and preventing cell injury.

BACKGROUND/AIMS: Essential hypertension is the most common cardiovascular disease and is involved in the development of the various cardiac arrhythmias, including atrial fibrillation. Recently, several studies have shown that statins have anti-arrhythmic effects, including the prevention of atrial fibrillation. This study investigated the effects of statins on cardiac electrophysiologic remodeling in patients with essential hypertension using the signal-averaged electrocardiogram (ECG) and standard 12-lead ECG. METHODS: This prospective multicenter study enrolled 115 patients with hypertension. Various antihypertensive drugs were administered alone or in combination according to their blood pressure. Statins were administrated in 56 patients. Laboratory tests, a standard 12-lead ECG, and signal-averaged ECG were performed at 1, 3, 6, and 12 months. Statistical analysis was performed using paired and independent t-tests and repeated measures analysis of variance (ANOVA). RESULTS: There was no significant difference in the clinical characteristics of the patients with and without statins. After antihypertensive therapy for 1 year, the P wave dispersion, high-frequency low-amplitude (HFLA) signals in the QRS complex of less than 40 micronV, and T peak-to-end dispersion were increased significantly (p<0.001, p<0.05, and p<0.01, respectively) in the patients who were not taking statins, while these changes were not seen in the statin group. CONCLUSIONS: These results demonstrate that electrophysiologic remodeling was progressive in patients with essential hypertension, despite antihypertensive therapy. However, combination therapy with a statin may inhibit the deterioration of inhomogeneity in atrial refractoriness and conduction disturbance.
Antihypertensive Agents ; Arrhythmias, Cardiac ; Atrial Fibrillation ; Blood Pressure ; Cardiovascular Diseases ; Electrocardiography ; Electrophysiology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Hypertension ; Prospective Studies