Intermittent Hypoxia Increases Ganglionated Plexus Nerve Activity And Focal Atrial Fibrillation:Important Role Of Autonomic Factors

Objective:We tested the hypothesis that intermittent hypoxia results in glionated plexus (GP) hyperactivity that contributes to focal atrial fibrillation (AF).Methods:Multi-electrode catheters were attached to atria, and all pulmonary veins. The ventilators were adjusted to simulate the intermittent hypoxia for1hour as an acute intermittent hypoxia model. At the end of each hour,40ms of high-frequency stimulation (HFS;100Hz,0.01ms pulse width) was delivered2ms after atrial pacing (during the refractory period) to determine the AF threshold (AF-TH), atrial effective refractory period (ERP) at each site at baseline and after1hour intermittent hypoxia. one electrodes was attached to the anterior right GP (ARGP) so that HFS (20Hz,0.1ms pulse width) to this site induced sinus rate (SR) slowing. Neural activity was recorded from the ARGP.Results:(1)1hour intermittent hypoxia induced a decrease in AF-TH and atrial ERP at all sites (all P<0.05).(2) The SR slowing response induced by ARGP stimulation was facilitated by1hour intermittent hypoxia.(3) The frequency and amplitude of the neural activity recorded from the ARGP were markedly increased by1hour intermittent hypoxia.Conclutions:1hour intermittent hypoxia facilitated AF inducibility and the chronotropic responses to parasympathetic stimulation. Increasing of neural activity in the GP may be a mechanism underlying these results.