The Effect Of Nicotinamide Adenine Dinucleotide (NADH) To Electrical Remodeling In Atrial Fibrillation

Background-The pathophysiology underlying electrophysiological remodeling(ER) from rapid atrial rates is unknown. To elucidate elements of these mechanisms, we examined the effect of nicotinamide adenine dinucleotide (NADH) on ER.Methods- Twenty-four rabbits were randomly divided into four groups(n=6 for each). The hearts were removed and perfused by the Langendorff technique with corresponding buffer continuously, respectively. At the same time, pacing the right atrium was performed for 1hour in all groups but not in control group. Before and after pacing, atrial effective refractory period(AERP) was determined in all hearts. Right atrium tissue was obtained for measurement of calcium-handling proteins mRNA using Semiquantitative Reverse Transcription-Polymerase ChainReaction(RT-PCR).Results- After pacing 1 hour, AERP shortened significantly in pacing/control group and pacing/NADH+rotenone group. but in pacing/NADH group, AERP did not obviously change. The mRNA level ofL-type Ca2+ channel aj subunit and sarcoplasmic reticulum calcium ATPase decreased and the mRNA level of ryanodine receptor type 2 increased in pacing/control group, but these changes were not found in pacing/NADH group.Conclusion-Activation of NADH is one mechanism underlying short-term ER.