Effects of transplantation on atrioventricular nodal accommodation and hysteresis

Tuna, Ishik C.; Barragry, T. P.; Walker, Marion; Lillehei, T. J.; Blatchford, J. W.; Gornick, Charles C.; Ring, W. Steves; Bolman, R. Morton; Benditt, David G.

doi:10.1152/ajpheart.1987.253.6.h1514

Cited by 6 publications

(8 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Tuna et al reported that the AV conduction time was delayed by the increase of the heart rate for the AV accommodation in dogs [13]. Therefore, it is necessary to regulate artificially the atrial rate for estimating the AV conductive function by the PR intervals.…”

Section: Discussionmentioning

confidence: 99%

Intrinsic Atrioventricular Conductive Function in Horses with a Second Degree Atrioventricular Block.

Yamaya

Kubo

Amada

et al. 1997

The Journal of Veterinary Medical Science

View full text Add to dashboard Cite

ABSTRACT. The atrioventricular (AV) conductive functions were investigated before and after the pharmacological autonomic nervous blockade (PAB) through the electrophysiological study on six horses (AV block group) in which the dropped beats occurred more frequently (over 200 beats/24 hr) and on five horses (control group) in which the dropped beats occurred sporadically (under 200 beats/24 hr) or in which the arrhythmias were not recognized at all on the long-term electrocardiogram. As a result, AV conductivity, conduction time and refractoriness in the AV block group were lower, longer and higher, respectively, than those in the control group even after PAB. These results indicate the intrinsic AV conductive functions in the AV block group were withdrawing than in the control group. -KEY WORDS: AV block, AV conduction, equine.J. Vet. Med. Sci. 59(3): 149-151, 1997 24 hr), and five horses (control group: 2-7 years old, 2 male and 3 female), with the dropped ventricular beats (under 200 beats/24 hr) or with no arrhythmias at all on the long-term electrocardiogram, were examined. As the higher right atrial pacing, a 7F electrode catheter was inserted from the upper left jugular groove by the vein stab method after the local anesthesia with lidocaine. The electrocardiogram was recorded with A-B lead at 50 mm/ sec paper speed and the atrial rate and PR interval before the atrial pacing were measured. Then the right atrial pacing was performed by stepwise increase of one minute duration at rate of 10 pulses/min from a few higher rate than the atrial rate by 200 pulses/min. To understand the AV conductivity and conduction time, Wenckebach rate, the mean PR interval and the mean RR interval were measured. Wenckebach rate was the pacing rate when a AV block occurred. The mean PR interval and the mean RR interval were calculated from all PR intervals and RR intervals during one minute atrial pacing at 100 pulses/min also. Then, to understand the refractoriness of AV conduction, the shortest RR interval during atrial pacing was also extracted from RR intervals at each pacing rate [17].The above-mentioned study was repeated 5 minutes after intravenous injections of propranolol (0.3 mg/kg) and atropine (0.04 mg/kg) by the PAB. The percentage alterations in all parameters, furthermore, were calculated to estimate the participant degree of the autonomic nervous system to AV conduction. The mathematical equation used was (after PAB -before PAB)/after PAB × 100.Measured values are presented as mean ± standard error. Statistical comparisons between means of parameters in the control and the AV block group or those before and after PAB in each group were made using the Student's paired t test. Probability of 5% or less was taken to indicate the statistical significance. Atrioventricular (AV) block is induced by the conduction disturbance of AV conduction system and roughly classified into the incomplete and complete AV block. The former incomplete AV block is frequently recognized in horses and the incidence of the second deg...

show abstract

Section: Discussionmentioning

confidence: 99%

Intrinsic Atrioventricular Conductive Function in Horses with a Second Degree Atrioventricular Block.

Yamaya

Kubo

Amada

et al. 1997

The Journal of Veterinary Medical Science

View full text Add to dashboard Cite

show abstract

“…For example, when atrial pacing decreases cardiac cycle length, the AV interval lengthens [3,4,[8][9][10]. Neither the autonomic blockade nor cardiac denervation affects the response in AV conduction, supporting an intracardiac origin of the cycle length dependent effect [4,[8][9][10]. Although both extrinsic autonomic and intrinsic mechanisms that have opposite influences on AV conduction are considered to regulate AV conduction time, their relative contribution during exercise in the daily life of humans remains to be solved.…”

Section: Introductionmentioning

confidence: 99%

“…On the other hand, an intrinsic mechanism that the AV node has affects AV conduction time as opposed to an alteration in sinoatrial rhythm. For example, when atrial pacing decreases cardiac cycle length, the AV interval lengthens [3,4,[8][9][10]. Neither the autonomic blockade nor cardiac denervation affects the response in AV conduction, supporting an intracardiac origin of the cycle length dependent effect [4,[8][9][10].…”

mentioning

confidence: 95%

Variability of Ventricular Excitation Interval Does Not Reflect Fluctuation in Atrial Excitation Interval during Exercise in Humans: AV Nodal Function as Stabilizer

Nakamoto

Matsukawa

2006

J. Physiol. Sci

View full text Add to dashboard Cite

Abstract:We have recently reported that the atrioventricular (AV) nodal mechanism functions to cancel fluctuation in the atrial excitation interval during a stair-stepping exercise. However, it remained unknown at which level of heart rate (HR) this mechanism started to operate and whether fluctuation in the interval might influence AV conduction over the following beats. To solve these questions, the variability of PP, RR, and PR intervals and their interrelationships were analyzed throughout ergometer exercise in eight subjects. The variability of the RR interval decreased to 0.7% of the control at 160 beats/min during exercise, much more than the PP interval variability, which decreased to 10%, despite the same shortened average interval. In contrast, the PR interval variability tended to increase by 87% during exercise, but the mean PR interval decreased. A strong inverse relationship between PP and the subsequent change in PR [∆PR] intervals became evident during exercise, implying that the ∆PR interval canceled fluctuation in the PP interval. However, there was little correlation between the RR and ∆PR intervals and between the PP interval and the next PR intervals in the forthcoming beat. When the slope of the PP-∆PR relationship, considered as sensitivity of the AV nodal function opposing an alteration in the PP interval, was plotted against the PP interval, the AV nodal function curve was approximated to a sigmoidal curve having a threshold of PP interval near 650 ms and a maximum plateau level of the slope near 1.0. We conclude that when HR exceeds 90-100 beats/min during dynamic exercise, the AV nodal mechanism will function to cancel fluctuation in the PP interval within one beat and keep the RR interval constant.Key words: extrinsic autonomic nerve activity, intrinsic mechanism of the AV node, heart rate variability, PR interval, dynamic ergometer exercise.The atrioventricular (AV) node plays an important role in producing a time delay between atrial and ventricular excitation to ensure appropriate ventricular filling. The AV conduction time is monitored as a PR interval from an electrocardiogram (ECG) or as a time interval between atrial and ventricular or His-bundle potentials from intracardiac electrodes. The beat-to-beat changes in AV conduction are controlled by both extrinsic and intrinsic mechanisms [1][2][3][4]. Both divisions of the autonomic nervous system richly innervate the AV node [2,5,6]. Stimulation of the cardiac sympathetic nerve facilitates AV conduction, whereas cardiac parasympathetic nerve stimulation impedes AV conduction [1,2,7]. Thus the neurogenic alterations in AV conduction occur in parallel with the changes in sinoatrial rhythm. On the other hand, an intrinsic mechanism that the AV node has affects AV conduction time as opposed to an alteration in sinoatrial rhythm. For example, when atrial pacing decreases cardiac cycle length, the AV interval lengthens [3,4,[8][9][10]. Neither the autonomic blockade nor cardiac denervation affects the response in AV conduction, suppo...

show abstract

“…However, in control dogs (i.e., innervated hearts) there was an asymmetry in the times for the A-H interval to reach steady state during increases and decreases in pacing rate of equal magnitude. 7 Based on these findings, it was postulated that this difference was probably due to asymmetrical neural influences on AV node function. 7 …”

mentioning

confidence: 99%

“…7 Based on these findings, it was postulated that this difference was probably due to asymmetrical neural influences on AV node function. 7 …”

mentioning

confidence: 99%

Atrioventricular nodal accommodation in isolated guinea pig hearts: physiological significance and role of adenosine.

Jenkins

Belardinelli

1988

Circulation Research

View full text Add to dashboard Cite

The progressive prolongation of atrioventricular node (AVN) conduction time to a new steady-state value caused by sadden and maintained increases in atrial rate is the most common form of AV nodal accommodation. This study was undertaken to 1) characterize AV nodal accommodation in isolated perfused guinea pig hearts, 2) investigate the influence of potential modulators of this phenomenon such as acetylcholine and adenosine, and 3) determine the physiological significance of AV nodal accommodation on cardiac function. Beat-by-beat changes in AVN conduction time caused by single-or multiple-step increases in atrial pacing rate were measured during control conditions and in the presence of atropine (1 fiM), propranolol (1 /uM), and the adenosine antagonist BW-A1433 (1 fiM). BW-A1433 was the only intervention that significantly reduced the cumulative and frequency-dependent prolongation of AVN conduction time but this was only observed at atrial cycle lengths £ 170 msec. In addition, BW-A1433 shortened the Wenckebach cycle length from 163 ±2 to 153 ±2 during normoxia and from 172 ±3 to 164 ±4 during mild hypoxia. In contrast, dipyridamole (1 fiM), an adenosine uptake blocker, markedly accentuated the AVN conduction time prolongation, accentuated the AV block associated with fast atrial rates, and significantly increased the Wenckebach cycle length. These effects of dipyridamole were prevented and antagonized by BW-A1433 and adenosine deaminase. When O 2 supply was limited and at the same time demand increased secondary to fast atrial pacing, the rate of adenosine release increased from a control of 125 ±27 to 580 ±54 pmol/min/g. This was accompanied by a significant prolongation in AVN conduction time that invariably progressed to AV block. Once AV block occurred, O 2 consumption decreased, O 2 supply-to-demand ratio improved and the rate of adenosine release dropped to 310 ±61 pmol/min/g. Reversal of the AV block with adenosine antagonists resulted in a decrease in O 2 supply-to-demand ratio and a severalfold increase in the rate of adenosine release. In this feedback system, adenosine signals the imbalance between O 2 supply and demand, causes AV block and, thus, reduces demand to compensate for the limited O 3 supply. On the other hand, adenosine deaminase and antagonists act as "error signals" by attenuating the effect of adenosine, whereas dipyridamole enhances the "gain" of the system by potentiating the effects of adenosine. We concluded that 1) AV nodal accommodation is an intrinsic property of the AVN that can be influenced by adenosine, and 2) under conditions of low O 2 supply-to-demand ratio, adenosine is produced as a negative feedback signal that protects the ventricles from excessive work by causing AV block. The wellrecognized dependence of AV conduction time on rate is consistent with this delay in recovery of excitability of the nodal cells. Furthermore, as also reported by Merideth et al, 1 the rate-dependency of AV transmission is cumulative, which indicates that the delayed recovery of excitab...

show abstract

Effects of transplantation on atrioventricular nodal accommodation and hysteresis

Cited by 6 publications

References 0 publications

Intrinsic Atrioventricular Conductive Function in Horses with a Second Degree Atrioventricular Block.

Intrinsic Atrioventricular Conductive Function in Horses with a Second Degree Atrioventricular Block.

Variability of Ventricular Excitation Interval Does Not Reflect Fluctuation in Atrial Excitation Interval during Exercise in Humans: AV Nodal Function as Stabilizer

Atrioventricular nodal accommodation in isolated guinea pig hearts: physiological significance and role of adenosine.

Contact Info

Product

Resources

About