Anti-oxidative stress effects of L-carnitine on acute atrial electrical remodeling in dogs

AIM: To evaluate the anti-oxidative stress effects of L-carnitine (L-CN) on tachycardia-induced acute atrial electrical remodeling in dogs. METHODS: Eighteen dogs were randomly divided into three groups: normal saline (NS) group, L-CN group and normal control (NC) group. In both NS and L-CN groups, right atrium was paced at 600 beats per minute (bpm) to induce atrial fibrillation (AF) and maintained for 2 h; 0.9% normal saline (300 mg/kg, IV) or L-carnitine (300 mg/kg, IV) was given before the pace and 0.9% normal saline or L-carnitine ［2.5 mg/(kg·min), 50 ml/h, ID］ was administered for 2 h. The observed atrial electrophysiology indexes included atrial effective refractory period (AERP), index of the AERP rate adaptation (AERP200/AERP150)/50 msec, conduction velocity (CV) and AF induced rate. Oxidation index of malondialdehyde (MDA) and antioxidation index of superoxide dismutase (SOD) of venous blood were measured before and 1 and 2 h after AF was measured. RESULTS: AERP shortened dramatically 2 h after AF (P<0.01) in NS group but no remarkable change was found in L-CN group. AERP rate adaptation in the right atrium decreased significantly (P<0.01) in NS group but did not change obviously in L-CN group. The AF-induced rate in L-CN group was significantly reduced (P<0.01). The oxidation index level (MDA) was increased and anti-oxidation index level (SOD) was decreased in both NS group and L-CN group (P<0.05). L-CN group had a lower MDA level and a higher SOD level compared with those in NS group (P<0.01). CONCLUSION: L-CN prevents tachycardia-induced oxidative stress and acute atrial electrical remodeling in dogs, possibly by cleaning the reactive oxygen species and inhibiting lipid peroxidation.