Certain evidence points to a role of inflammation in AF pathophysiology. Thus, antiinflammatory treatment of AF is discussed. Effects of a dexamethasone treatment (7 days) on atrial ion currents (I Ca,L , I to, I sus ) and their tachycardia-induced remodeling were studied in a rabbit model. Methods: 6 groups of 4 animals each were built. Rapid atrial pacing (600 min) was performed for 24 and 120 hours with/ without dexamethasone treatment. Ion currents were measured using whole cell patch clamp

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... method. Results: Rapid atrial pacing reduced I Ca,L . I to was decreased after 24 hours but almost returned to control values after 120 hours. When dexamethasone-treated animals also underwent atrial tachypacing, pacing-induced reduction of I Ca,L was still observed after 24 hours and was even augmented after 120 hours compared to untreated but tachypaced animals. I to was not influenced by dexamethasone alone. In dexamethasone-treated animals, reduction of I to was not observed after 24 hours but occurred after 120 hours of atrial tachypacing. I sus was neither influenced by rapid atrial pacing nor by dexamethasone. Biophysical properties of all currents were affected neither by rapid atrial pacing nor by dexamethasone. Conclusion: Dexamethasone influenced tachycardia-induced alterations of atrial I to . Our experiments give evidence that -amongst other anti-inflammatory action -impact of dexamethasone on ion currents and their tachycardia-induced alterations might also play a role in treatment/prevention of AF with steroids.