Biomedical subjects

J Billette

Publications and source records attributed to J Billette.

35 records · Page 2Linked to original sources

PubMed1988

Selective functional characteristics of rate-induced fatigue in rabbit atrioventricular node.

The slowly developing rate-induced prolongation in atrioventricular nodal conduction time, termed "fatigue," was selectively studied using specifically designed stimulation protocols in isolated rabbit heart preparations. A nodal recovery curve (A2H2 versus H1A2 intervals; nodal conduction time of each premature beat plotted against corresponding recovery time) was obtained before and after a stable and nearly maximum fatigue had been reached by driving the atrium for 5 minutes at a fast rate close to the upper limit of 1:1 nodal conduction. The fatigue uniformly prolonged all A2H2 intervals (12.3 +/- 1.3 msec) and systematically increased the minimum H1A2 interval at which complete nodal block occurred (24.8 +/- 4.0 msec) (p less than 0.01, n = 6). To study the rate and time dependence of fatigue, nodal conduction times were obtained during three rapid 5-minute pacings corresponding to 50%, 75%, and 100% shortening of the pacing interval in the 1:1 nodal conduction range. The respective maximum fatigue-induced increases in conduction time were 5.4 +/- 1.8, 9.0 +/- 2.7, and 12.5 +/- 2.1 msec (p less than 0.01, n = 6). However, the pacing interval had no significant effect on the time required to reach either 50% (17.1 +/- 3.5 seconds) or 90% (92.6 +/- 15.4 seconds) of the fatigue observed after 5 minutes of fast rate. At the termination of any rapid stimulation, the fatigue effect dissipated with a time course that was inverse but symmetrical to that of its induction. These findings support the existence of an independent, slow, nodal memory process by which the conduction time changes according to past events with a long time constant.

Animals↗

PubMed1987

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

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 less than 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 less than 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).

Animals↗

PubMed1987

Atrioventricular nodal activation during periodic premature stimulation of the atrium.

To study the intranodal origin of the functional properties of the atrioventricular node, progressive changes in nodal cell activation time and cycle length occurring during complete sequences of periodic premature stimulation of the atrium were determined for 419 nodal cells recorded in 11 isolated rabbit heart preparations. The conduction time in proximal nodal cells including the N cells increased only at very short coupling intervals. Conduction time in the distal node (NH and H cells) first increased and then decreased with increasing prematurity. The major fraction of the basic and premature delays developed between N and NH cell activation, a period devoid of upstrokes. The effective and functional refractory periods were related to the minimum intervals between successive upstrokes at the node entrance and outlet, respectively. These results suggest that the cycle-length dependency of nodal conduction is the result of complex changes in propagation time occurring at three levels in the node, whereas the effective and functional refractory periods reflect reactivation limits of cells located at the node entrance and outlet, respectively.

Action Potentials↗

PubMed1986

Common functional origin for simple and complex responses of atrioventricular node in dogs.

The possibility that variations in atrioventricular nodal conduction time observed during transient and steady-state nodal responses share common characteristics was examined in six anesthetized dogs. Atrioventricular conduction times (AV intervals) obtained during transient (incremental atrial pacing rates, short frequency steps, and Wenckebach cycles) and steady state (periodic premature stimulation performed at 5 basic rates) responses were plotted together against the corresponding preceding ventriculoatrial (VA) intervals on a graph for each dog. Despite their diversity, nodal responses consistently resulted in AV intervals that fell within a well-defined, relatively narrow, crescent-shaped zone on the graphs. AV interval variations were small in the long VA interval range and increased slightly but predictably as the VA intervals decreased. AV intervals of transient and steady state nodal responses overlapped markedly. These results show that AV intervals of transient and steady-state nodal responses vary within a given common functional domain despite the diversity of their sequential patterns and suggest that the AV node may be obeying the same set of conduction rules during these very distinct responses.

Animals↗

PubMed1984

Effects of sino-atrial ischaemia on the heart rate response to phasic burst stimulation of the right cervical vagus in the dog.

The effects of occluding sinus node arteries on the pacemaker responses to graded phasic burst stimulation of the right cervical vagus were studied in anaesthetised dogs. In six dogs (Group I), phase response curves (vagally affected atrial cycle plotted against the phase of the stimulus in the cycle) to 1, 3 and 5 pulse burst stimulations were determined at control and hourly for 3 h after the occlusion. In four dogs, the occlusion produced a slowing of the heart rate, a shift of pacemaker outside sinus node region and a displacement of the phase response curves upward and to the right. Identical stimulation bursts resulted in significantly longer atrial cycles than at control, and bursts introduced with a longer phase remained effective and resulted in significantly longer atrial cycles than the maximum one reached at control. However, when the vagal responses were corrected for occlusion-induced changes in spontaneous PP intervals, the occlusion was found not to significantly affect the vagal responses except to increase their variability. Time-related differences in the effects of the occlusion were not statistically significant. In six control dogs (Group II) submitted to the same protocol, occlusion excepted, the vagal response curves changed very little over the 3 h experiments, thus confirming the stability of the experimental preparation used and of the vagal responses obtained in the absence of ischaemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1984

Effects of diltiazem on atrioventricular conduction and arterial blood pressure: correlation with plasma drug concentrations.

Atrial and atrioventricular conduction variables were studied at control and at the end of each of six consecutive 45-min diltiazem administration periods in eight closed chest-anesthetized dogs. Diltiazem was given as a bolus (50 micrograms/kg, i.v.) followed by an infusion (0.5 micrograms X kg-1 X min-1); doses were doubled in subsequent periods. The plasma concentrations, measured by gas-liquid chromatography, ranged from 8 to 1400 ng/mL and correlated strongly with the doses (r = 0.92; p less than 0.01). The Wenckebach cycle length, basic conduction time, and functional refractory period of the atrioventricular (AV) node increased proportionally with plasma concentration (respective r = 0.90, 0.89, 0.80; p less than 0.01). The minimum mean plasma concentrations affecting these variables significantly were 37, 83, and 175 ng/mL, respectively. Second or third degree AV blocks developed in all dogs for plasma concentrations between 379 and 1400 ng/mL. In four dogs which were given isoproterenol (0.2 micrograms X kg-1 X min-1), these blocks disappeared within 1 min. Atrial conduction time and functional refractory period were slightly but significantly shortened by diltiazem with mean plasma concentrations of 175 ng/mL and over. His-Purkinje intervals were not significantly changed by diltiazem. Systolic and diastolic arterial pressures were decreased by diltiazem (r = -0.64, r = -0.79; p less than 0.01) starting with a mean plasma concentration of 83 ng/mL. We conclude that AV nodal conduction variables are progressively prolonged with increasing plasma concentrations of diltiazem; plasma concentrations affecting blood pressure and AV nodal variables overlap; and the AV blocks produced by toxic concentrations of diltiazem can be corrected by isoproterenol.

Animals↗

PubMed1981

Short time constant for rate-dependent changes of atrioventricular conduction in dogs.

The number of short cardiac cycles necessary to induce, and normal cycles to dissipate, a rate-dependent shortening in atrioventricular (AV) nodal functional refractory period (FRP) and conduction time (CT) was determined in six anesthetized dogs. For the induction study, the periodic premature stimulation procedure was performed at control and repeated six times while 1, ..., 6 conditioning short prepremature cycles (PPC) were introduced between the last basic cycle and the premature cycle. In all dogs, FRP was maximally shortened and the recovery curve was maximally shifted to the left when the premature cycle was preceded by 1 PPC. Adding 2, ..., 6 PPC resulted in slightly fewer but persistent shortenings of both FRP and CT. The dissipation of the FRP and CT shortenings produced by 2 and 6 PPC was studied subsequently in the same dogs by introducing 1, ..., 6 normal basic cycles between the last PPC and the test premature cycle. The FRP and CT shortenings induced by 2 or 6 PPC were almost completely dissipated after one normal basic cycle. Thus, one short cycle produces a maximum shortening in AV nodal FRP and CT, and one normal basic cycle is sufficient to dissipate these effects.

Animals↗

PubMed1979

A microcomputer-based stimulator for clinical and experimental investigations in cardiac electrophysiology.

A cardiac stimulator is described which combines the ease of operation required in clinical investigations, particularly endocavitary studies of cardiac arrhythmias, and the versatility needed in a research context. This instrument uses a microcomputer to control two independent optically-isolated stimulation ports which can be addressed either independently or jointly to stimulate at two different sites. The main software module operates as a cascade of ten real time pulse generators with individually presettable parameters: amplitude, duration, period, initial delay, periodic and cyclic modifiers, triggering mode, etc. A simple interactive procedure allows the operator to define a stimulation protocol either by accessing the generator structure directly, or by calling any of five pre-programmed stimulation protocols. With this combination, the instrument can provide a large variety of pulse patterns. The operator can intervene at any time during stimulation to change parameter values or modify the pulse pattern. Concurrently with stimulation, the instrument generates time-codes to help relate cardiac responses recorded on paper chart and magnetic tape, and reference them to specific events. The instrument can be readily expanded by the addition of parallel microprocessor modules; other real time tasks such as acquisition and processing of cardiac responses can thus be incorporated.

Cardiac Pacing, Artificial↗

PubMed1978

Acute ischemic sinus node dysfunctions in dogs.

The effects of the occlusion of the two main atrial arteries irrigating the sinus node on sinus rhythm and postpacing sinus recovery were studied in 12 anesthetized dogs. Records of spontaneous rhythm and of postpacing sinus recovery were taken at control and hourly for 6 hours after the occlusion. The spontaneous cycle length (AA interval) was 335 +/- 11 ms at control and 416 +/- 17 ms (mean +/- SE) (p less than 0.005) one hour after the occlusion. It remained nearly unchanged during the following 5 hours of observation. The occlusion also shortened atrioventricular conduction time (AV interval) and reduced P-wave amplitude in ECG lead II in 9 of these dogs. While the control postpacing sinus recovery time was 397 +/- 13 ms, the 1-hour value was 715 +/- 165 ms. This prolongation persisted during the first four postocclusion hours but was less marked during the last two hours of observation. Moreover, the postpacing mode of return of the AA intervals to their prepacing value (sinus recovery pattern) became characteristically slow and progressive after occlusion, complete postpacing recovery often occurring only after 100 or more beats. Sequences of escape atrial and/or AV junctional rhythms were frequently seen during this recovery. Atrial extrasystoles and short sequences of atrial tachycardias were observed in most dogs after occlusion. Conversely, none of these changes occurred during a 6-hour experimental time in 5 control dogs in which the same protocol, occlusion excepted, was repeated. These observations show that the sinus node function in the dog is consistently affected by impairing its blood supply. Ischemic dysfunctions include sinus slowing, pacemaker shift, prolonged sinus recovery time, delayed postpacing recovery and supraventricular tachyarrhythmias.

Animals↗

PubMed1976

Preceding His-atrial interval as a determinant of atrioventricular nodal conduction time in the human and rabbit heart.

This investigation shows that atrioventricular (A-V) nodal conduction time (A-H interval), both in the human and in the isolated rabbit heart, is determined mainly by the length of the preceding His-atrial (H-A) interval. The A-H intervals obtained during atrial extrasystolic stimulation at different basic rates, during Wenckebach cycles and during both transient and steady state responses to stepwise increases in stimulation frequency were plotted against the corresponding H-A intervals. The A-H intervals were found to have nearly the same duration provided they were preceded by the same H-A interval. The only important difference appeared in the short H-A interval range as a shortening of the A-H interval at faster basic rates. This facilitating effect of frequency, which was found in the majority of cases, is compatible with the similarly frequency-dependent shortening of the functional refractory period of the A-V node.

Animals↗

PubMed1976

Cycle-length-dependent properties of AV nodal activation in rabbit hearts.

Cycle-length-dependent changes in AV nodal cell activation were studied in isolated preparations from rabbit hearts. Transmembrane action potentials were recorded from the node while it was propagating impulses initiated in the atrium with an accelerating train of stimuli. This train consisting of five successive stimuli separated by progressively shorter intervals was uniformly repeated at every 10th basic beat, each time reproducing a sequence of five different increasing AV nodal delays. The AN and NH cells were found to contribute only slightly to the cycle-length-dependent AV nodal delay which developed mainly in the small N zone, located centrally in the AV node. With the increasing delay, the action potentials from this N zone typically dissociated into two components synchronous with late AN and early NH activity, respectively. The amplitude of the first component decreased, wheareas that of the second increased progressively in N cells activated progressively later. No cells were activated at an intermediate time between the two components. This dissociation was not accompanied by changes in the activation pattern of the AV node. The different nodal cells classified according to their response to the accelerating train delineated functional zones corresponding to different anatomic structures. The possible mechanisms which would explain the cycle-length-dependent AV nodal delay are discussed.

Action Potentials↗

PubMed1975

Roles of the AV junction in determining the ventricular response to atrial fibrillation.

The statistical properties of RR interval sequences during cholinergic atrial fibrillation were studied in anesthetized dogs both in control conditions and after the selective injection of dromotropic agents into the atrioventricular (AV) node artery. It was observed that RR interval histogram configurations depended mainly on the mean heart rate, regardless of whether it was a control or a post-injection sequence. The sequences were found to vary from almost regular at fast rates to highly irregular at slow rates, covering all intermediate possibilities. Since the injections of dromotropic agents into the AV node artery were carried out during sinus rhythm between the episodes of fibrillation, their influences on the AV junction, as reflected both on the length of the PR interval during sinus rhythm and on the RR interval dispersion during fibrillation, could be compared. The dispersion of RR intervals was found to increase as the PR interval duration became longer. In addition, it was observed that the generally random character of the RR interval sequences during fibrillation was not affected by the injection of dromotropic agents into the AV node artery. These results were interpreted as an indication that, for a well-established atrial fibrillation, the degree of ventricular irregularity (dispersion of RR intervals) is related to the conductivity within the AV junction and that the random character of RR interval sequences is related to the atrial fibrillatory activity itself.

Acetylcholine↗

PubMed1974