| BackgroundAtrial fibrillation (AF) is a common arrhythmia with a prevalence of 0.4% to 0.9% in the population. Its incidence increases with age. The course of atrial fibrillation can be classified to paroxysmal atrial fibrillation and chronic atrial fibrillation (including persistent atrial fibrillation and permanent atrial fibrillation). Most of patients with paroxysmal atrial fibrillation often progresses to chronic atrial fibrillation with different transform ratio by different pathogenesis. The duration of the paroxysms of atrial fibrillation was found to be of importance, transition to chronic atrial fibrillation occurring in 31% of patients with paroxysms shorter than 2 days versus 46% if the episodes of atrial fibrillation were of longer duration.There may be a mechanism to maintain atrial fibrillation or relapse during the course from paroxysmal atrial fibrillation to chronic atrial fibrillation. Katz's divided the influence of heart by atrial fibrillation into three types, they are metabolic change (on the cell), ion channel change (on the gene) and structure change (on the organ). The fastest change is on the metabolism which occurs from a few seconds to a few minutes. The ion concentration in the cells, the activity of ion pump and the phosphorylation of ion channel will be changed. And the electrophysiological remodeling will happenwhen the atrial fibrillation sustains a few hours or a few days. The atrial myocardium cells will remodel after a few weeks. Then long-term atrial fibrillation will cause irreversible structure destroy.The electrophysiological remodeling caused by atrial fibrillation is one of the reasons which beget the maintain of atrial fibrillation and develop to the sustained atrial fibrillation. It's just called "Atrial Fibrillation Begets Atrial Fibrillation". And the structure remodeling caused by atrial fibrillation is an important factor which leads the atrial contractile dysfunction after sustain atrial fibrillation defibrillation. So in recent studies indicate that the electrophysiological and structure remodeling is the most character of atrial fibrillation.Previous studies show that the Na+/H+ Exchanger subtype 1 (NHE-1) take part into the regulation of Calcium in the myocardium cells, and the activity of NHE-1 is one of the mechanisms of the short-term electrophysiological remodeling and the structure remodeling. Some evidence indicates that atrial myocardium cells have intracellular acidosis because is hypoxia during short-term atrial fibrillation. The Na+/H+ Exchanger Inhibitors (NHEIs) prevent the Na+ overload and the secondary Ca2+ overload caused by intracellular acidosis. So it prevents the electrophysiological remodeling.There is no report about atrial eletrophysiological remodeling effects of NHEI. The purpose of this study was to test the atrial electrophysiological remodeling effects of Cariporide, a selective blockade of the cardiac NHE-1 isoform, in short-term rapid atrial pacing on rabbit, and suspect the mechanism of NHE-1 in atrial electrophysiological remodeling. Materials and Methods 1, Study subjectsTwenty adult rabbits (2.2 to 2.9 kg) were selected. The control group was injected the solvent of Cariporide, and the experimental group was injected the Cariporide.2 Equipment and reagentCF-4 multifunction cardiac electrophysiological programmed stimulator, EP Laboratory LabSystem DUO multi-channel electrophysiological recorder, DSA, Cordis electrode catheter, Venous hook, Injection micro pump, Transfer micro pipe, Cariporide, DMSO, Urethane, Metoprolol tartaric acid, atropine hydrochloride, 3 MethodsRabbit was anesthetized with a bolus dose of 20% urethane (5ml/kg IV) and fixed on the operation table. The internal jugular vein and external jugular vein were isolated, and two Cordis electrode catheter were insert into the right atrium via them. One is used to pace right atrium, another is used to record right atrium electrogram. Next, the recording electrode was connected to the multi-channel electrophysiological and the pac... |
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