Mechanism of atrioventricular nodal facilitation in rabbit heart: role of proximal AV node

• Published in: The American journal of physiology Vol. 273; no. 4; pp. H1658 - H1668
• Main Authors: Mazgalev, T, Mowrey, K, Efimov, I, Fahy, G J, Van Wagoner, D, Cheng, Y, Tchou, P J
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01-10-1997
• Subjects: Animals; Atrial Function; Atrioventricular Node - cytology; Atrioventricular Node - physiology; Bundle of His - physiology; Cardiac Pacing, Artificial; Electrophysiology - instrumentation; Electrophysiology - methods; Female; Heart - physiology; Male; Microelectrodes; Rabbits
• ISSN: 0002-9513; 2163-5773
• DOI: 10.1152/ajpheart.1997.273.4.h1658

The phenomenon of atrioventricular (AV) nodal "facilitation," described in traditional "black box"-functional studies, implies enhanced AV nodal dromotropic function. We investigated the role of atrial prematurities in the modulation of the nodal cellular responses in the mechanism of AV nodal facilitation. Atrial and His (H) bundle electrograms and microelectrode recordings from proximal AV nodal cells were analyzed in 15 superfused rabbit AV node preparations. The pacing protocol consisted of 30 basic beats (S1; coupling interval S1-S1 = 300 ms) followed by a facilitating prematurity (S2; coupling intervals S1-S2 of 300, 200, 150, and 130 ms) followed by the test beat (S3; coupling interval S2-S3 scanned in 5-ms steps). Conduction curves (S2-H2 vs. S1-S2, S3-H3 vs. S2-S3, and S3-H3 vs. H2-S3) were constructed. Facilitation (i.e., shortening of S3-H3 when S1-S2 was shortened) was demonstrated in all preparations using the H2-S3 (P < 0.001) but not the S2-S3 format. Microelectrode recordings revealed a causal relationship between the improved proximal AV nodal cellular responses in facilitation and the prolonged S2-S3 interval. There was no evidence for enhanced nodal dromotropic function directly resulting from the introduction of the facilitating beats. Thus facilitation is based on inherent cycle-length-dependent properties of the AV node during application of a complex pacing protocol and primarily reflects the uncontrolled modulation of the proximal cellular response.