Objective To investigate the effect of omeprazole on the acute atrial electrical remodelling and oxidative stress status in rabbit atrial fibrillation (AF) model.

Methods 18 rabbits were randomly divided into atrial tachypacing (ATP) group, sham operating (SM) group, and atrial tachypacing with omeprazole therapy (A+O) group. In the ATP group and A+O group the right atrium was tachypaced at 500–600 bpm to induce and maintain AF for 3 h. The A+O group were given intravenous administration of omeprazole treatment (4 mg/kg) 15 min before tachypacing. The ATP group were given intravenous administration of physiological saline 10 ml 15 min before pacing. The SM group were not paced. The atrial electrophysiological indexes (AERP, Rate adaptive of AERP) were measured at different time point (baseline, 0.5 h, 1 h, 1.5 h, 2 h, 2.5 h and 3 h after pacing). Oxidative stress markers (SOD, MDA, T-NOS) in serum were measured at different time point (baseline and 3 h after pacing).

Results 1. Compare to SM group, the atrial effective refractory period (ERP) at a cycle length of 200 ms was decreased from 93.89±5.88 to 72.78±5.37 ms (p<0.01) after pacing in ATP group, and the Rate adaptive of ERP appeared non-performing significantly after tachypacing in ATP group (from 0.10±0.02 to 0.04±0.01, p<0.01); but no change in A+O group, with ERP and Rate adaptive of ERP averaging 100.17±8.93 ms and 0.09±0.02. The level of lipid peroxidation index --MDA increased significantly after tachypacing in ATP group (from 1.99±0.51 to 2.94±0.78 nmol/ml, p<0.05), but no change in A+O group. 2. Compare to the result at the same time in R+O group, the ERP shortened dramatically (p<0.05) after tachypacing in ATP group; The Rate adaptive of ERP appeared non-performing significantly after pacing in ATP group; The level of MDA increased (p<0.05) after tachypacing in ATP group.

Conclusion Omeprazole could effectively suppressed tachypacing-induced electrical remodelling in rabbit AF model and greatly attenuated the oxidative stress by downregulating lipid peroxidation.