Autonomic modification of the atrioventricular node during atrial fibrillation - Role in the slowing of ventricular rate

Background-Postganglionic vagal stimulation (PGVS) by short bursts of subth reshold current evokes release of acetylcholine from myocardial nerve termi nals. PGVS applied to the atrioventricular node (AVN) slows nodal conductio n. However, Little is known about the ability of PGVS to control ventricula r rate (VR) during atrial fibrillation (AF). Methods and Results-To quantify the effects and establish the mechanism of PGVS on the AVN, AF was simulated by random high right atrial pacing in 11 atrial-AVN rabbit heart preparations. Microelectrode recordings of cellular action potentials (APs) were obtained from different AVN regions. Five int ensities and 5 modes of PGVS delivery were evaluated. PGVS resulted in cell ular hyperpolarization, along with depressed and highly heterogeneous intra nodal conduction. Compact nodal AP exhibited decremental amplitude and dV/d t and multiple-hump components, and at high PGVS intensities, a high degree of concealed conduction resulted in a dramatic slowing of the VR. Progress ive increase of PGVS intensity and/or rate of delivery showed a significant logarithmic correlation with a decrease in VR (P<0.001). Strong PGVS reduc ed the mean VR from 234 to 92 bpm (P<0.001). The PGVS effects on the cellul ar responses and VR during AF were fully reproduced in a model of direct ac etylcholine injection into the compact AVN via micropipette. Conclusions-These studies confirmed that PGVS applied during AF could produ ce substantial VR slowing because of acetylcholine-induced depression of co nduction in the AVN.