Functional origin of rate-induced changes in atrioventricular nodal conduction time of premature beats in the rabbit

Abstract

The characteristics and origin of the rate-induced changes in atrioventricular nodal conduction time of premature beats (A₂H₂ intervals) were studied in isolated rabbit heart preparations. Increasing the basic driving rate during a periodic premature stimulation prolonged (a net inhibitory effect) and shortened (a net facilitatory effect) significantly (p < 0.01, n = 17) the A₂H₂ intervals associated with long and short recovery times (H₁A₂ intervals), respectively. The origin of these responses was sought for by analyzing interactions between facilitation and fatigue. When the fatigue developed at a fast basic rate was estimated from changes in conduction time of basic beats and subtracted from the corresponding A₂H₂ intervals, the calculated A₂H₂ intervals showed enhanced facilitation but no fatigue. When independently obtained fatigue and facilitation effects were added to the control A₂H₂ intervals for corresponding H₁A₂ intervals, resulting A₂H₂ intervals correlated strongly with the ones observed at the equivalent fast basic rate (r = 0.99, p < 0.001). Moreover, changes in the A₂H₂ intervals of premature beats tested with constant coupling intervals during 5-min fast rates were biphasic, confirming the overlapping and competition between facilitation and fatigue effects. Hence, rate-induced deviations of premature nodal conduction time from that predicted by changes in recovery time are consistent and result from the interaction between the overlapping effects produced by two independent, antagonist, and dynamically distinct nodal properties (facilitation and fatigue).