MECHANISM OF ATRIOVENTRICULAR NODAL FACILITATION IN THE RABBIT HEART - ROLE OF THE DISTAL AV NODE

We investigated whether atrioventricular (AV) nodal facilitation is th e result of distal AV nodal action potential shortening. Atrial and bu ndle of His (H) electrograms and microelectrode recordings from proxim al and distal AV nodal cells were analyzed in eight superfused rabbit AV node preparations in response to two pacing protocols. In the facil itation protocol, an atrial extrastimulus (A3) was preceded by an atri al impulse (A2) introduced 300, 200, 150, or 125 ms after 30 basic bea ts (A1). The preexcitation protocol differed from the facilitation pro tocol by the addition of a premature His depolarization (h2) such that the H1-h2 interval was shorter than the H1-H2 interval. Conduction cu rves (A3-H3 vs. H2-A3, h2-A3, and A2-A3 intervals) were constructed. F acilitation was demonstrated in all preparations when H2-A3 was used ( P = 0.02) but not in the A2-A3 format. Compared with facilitation at t he same A1-A2 intervals, preexcitation, despite shortening the distal cellular action potential duration, resulted in longer A3-H3 delays (P = 0.002), shorter A2-A3 intervals, and depression of the proximal nod al cellular response. Thus facilitation does not result from altered d istal AV nodal characteristics and instead is a manifestation of an un controlled pacing protocol-dependent modulation of proximal AV nodal f unction.