Role of nitric oxide on the electrophysiological properties of isolated rabbit atrioventricular node by extracellular field potential during atrial fibrillation

The aim of the present study was to determine direct effects of NO modulation on protective electrophysiological properties of atrioventricular node (AV node) in the experimental model of AF in rabbit. Isolated perfused rabbit AV nodal preparations were used in two groups. In the first group (N=7), LNAME (50μM) was applied. In the second group (N=12), different concentrations of L - argenine (250 μM - 5000 μM) were added to the solution. Programmed stimulation protocols were used to quantify AV nodal conduction time, refractoriness and zone of concealment. AF protocol was executed by software with coupling intervals (ranging from 75 – 125 msec). L-NAME had depressive effects on basic AV nodal properties. L-Arginine (250μM) had direct inhibitory effects on nodal conduction time, Wenckebach and refractoriness. Significant increases in the number of concealed beats were induced by L-Arginine (500 μM). Number of concealed beats were increased from 700.7 ± 33.7 to 763 ±21 msec (P<0.05). Trend of zone of concealment prolongation in a frequency-dependent model was abrogated by Larginine (250, 5000 μM). NO at low concentration (in the presence of L-NAME) had facilitatory role on AV nodal properties, but at high concentration (in the presence of L-arginine) enhanced protective role of AV node during AF. Biphasic modulatory role of NO may affect protective behavior of AV node during AF.