Influence of cardiac denervation on subsidiary atrial pacemaker stabilization

1984 ◽  
Vol 247 (4) ◽  
pp. H523-H530
Author(s):  
J. A. Sterba ◽  
L. E. Rinkema ◽  
W. C. Randall ◽  
S. B. Jones ◽  
G. Brynjolfsson

Overdrive suppression was determined by measuring cardiac cycle lengths after rapid atrial pacing in nine alert conscious dogs sustaining total intrapericardial denervation. Rapid atrial pacing was performed at 125-400% of spontaneous heart rate for 30 s and at 200% spontaneous rate for 30, 60, 120, and 180 s, with and without cholinergic (atropine 0.2 mg/kg iv) or adrenergic blockade (propranolol 0.5 mg/kg iv). Corrected recovery time (CRT) was defined as the first recovery cycle length minus average control cycle length. To compare responses of the intact sinoatrial node (SAN) and subsidiary atrial pacemakers, CRT was measured in the conscious animal before and after SAN excision. Immediately after SAN excision, a junctional rhythm was frequently observed, but within a short time (min-h), subsidiary atrial pacemaker dominance was established with well-formed P waves and P-R interval averaging 85.3 +/- 3.4 ms. CRT before SAN excision ranged from 100 to 300 ms. Following pacing at 125-400% of spontaneous heart rate soon after SAN excision, CRT was markedly prolonged, ranging up to 6,000 ms. Atropine and propranolol did not influence CRT in the denervated preparation. CRT of subsidiary atrial pacemakers in the normally innervated dog heart returned to control pre-SAN excision values in 1-2 wk. In the denervated heart complete autonomic denervation exaggerated time required for return to control CRT values to 5-8 wk.

1982 ◽  
Vol 53 (3) ◽  
pp. 631-636 ◽  
Author(s):  
I. Y. Liang ◽  
H. L. Stone

Diastolic coronary resistance (DCR) was determined in seven conscious dogs in the untrained state and after 4–5 wk of daily exercise conditioning (partial training). The conditioning regime consisted of treadmill running 5 days/wk. The dogs were instrumented to measure aortic pressure and left circumflex coronary flow during atrial pacing with implanted electrodes. Heart rate was varied from the resting value to 240 beats/min before and after adrenergic blockade with propranolol (beta B, 1 mg/kg) or phentolamine (alpha B, 1 mg/kg); myocardial oxygen consumption (MVO2) was measured in three dogs under the same condition in both the untrained (UT) and partially trained (PT) condition. DCR decreased with increasing heart rate [from 4.75 +/- 0.56 (SE) to 2.48 +/- 0.22 Torr . ml-1 . min at 240 beats/min]; alpha B reduced DCR, whereas beta B increased DCR. In the PT condition, DCR decreased to 4.02 +/- 0.40 Torr . ml-1 . min at rest and was decreased to 1.82 +/- 0.16 Torr . ml-1 . min at 240 beats/min (P less than 0.05 compared with UT). alpha-Adrenergic and beta-adrenergic blockade in the PT condition resulted in parallel reduction in DCR compared with the UT condition. MVO2 was unaffected by either PT or adrenergic blockade but increased as heart rate increased with atrial pacing. These data suggest a change in caliber of the coronary resistance vessel because of the parallel shift in the relationship between DCR and heart rate.


1975 ◽  
Vol 38 (6) ◽  
pp. 1110-1116 ◽  
Author(s):  
H. L. Stone

The relationship between heart rate and left atrial end-diastolic diameter (LAEDD) and left atrial systolic shortening (LASS) was investigated in 12 conscious dogs. Atrial pacing, vagal blockade, isoproterenol, and beta-adrenergic blockade were used to change heart rate and the inotropic state of the atrium. LAEDD decreased linearly as heart rate increased. LAEDD averaged 33.0 mm (+/- 0.6 mm SEM) and decreased by 3.2 mm (+/- 0.4 mm SEM) with a change in heart rate of 50 beats/min. The ratio of LASS/LAEDD decreased as LAEDD decreased with increasing heart rate, but there was less of a reduction in the ratio at the extreme levels of LAEDD change with isoproterenol and vagal blockade. Propranolol reduced LASS at any LAEDD. At lower heart rates the reduction of LASS with pacing could be corrected by returning LAEDD to near control levels with a rapid infusion of fluid. It is concluded that LASS is primarily dependent on LAEDD and the inotropic state of the atrium. At higher heart rates, though, some effect of frequency can be observed. Isoproterenol and vagal blockade (increased contractile state) reduced the dependence of LASS on LAEDD.


2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Matthias Daniel Zink ◽  
Christoph Brüser ◽  
Patrick Winnersbach ◽  
Andreas Napp ◽  
Steffen Leonhardt ◽  
...  

Background.Heart rate monitoring is especially interesting in patients with atrial fibrillation (AF) and is routinely performed by ECG. A ballistocardiography (BCG) foil is an unobtrusive sensor for mechanical vibrations. We tested the correlation of heartbeat cycle length detection by a novel algorithm for a BCG foil to an ECG in AF and sinus rhythm (SR).Methods.In 22 patients we obtained BCG and synchronized ECG recordings before and after cardioversion and examined the correlation between heartbeat characteristics.Results.We analyzed a total of 4317 heartbeats during AF and 2445 during SR with a correlation between ECG and BCG during AF ofr=0.70(95% CI 0.68–0.71,P<0.0001) andr=0.75(95% CI 0.73–0.77,P<0.0001) during SR. By adding a quality index, artifacts could be reduced and the correlation increased for AF to 0.76 (95% CI 0.74–0.77,P<0.0001,n=3468) and for SR to 0.85 (95% CI 0.83–0.86,P<0.0001,n=2176).Conclusion.Heartbeat cycle length measurement by our novel algorithm for BCG foil is feasible during SR and AF, offering new possibilities of unobtrusive heart rate monitoring. This trial is registered with IRB registration number EK205/11. This trial is registered with clinical trials registration numberNCT01779674.


2001 ◽  
Vol 204 (24) ◽  
pp. 4361-4366
Author(s):  
F. Seebacher ◽  
C. E. Franklin

SUMMARY During thermoregulation in the bearded dragon Pogona barbata, heart rate when heating is significantly faster than when cooling at any given body temperature (heart rate hysteresis), resulting in faster rates of heating than cooling. However, the mechanisms that control heart rate during heating and cooling are unknown. The aim of this study was to test the hypothesis that changes in cholinergic and adrenergic tone on the heart are responsible for the heart rate hysteresis during heating and cooling in P. barbata. Heating and cooling trials were conducted before and after the administration of atropine, a muscarinic antagonist, and sotalol, a β-adrenergic antagonist. Cholinergic and β-adrenergic blockade did not abolish the heart rate hysteresis, as the heart rate during heating was significantly faster than during cooling in all cases. Adrenergic tone was extremely high (92.3 %) at the commencement of heating, and decreased to 30.7 % at the end of the cooling period. Moreover, in four lizards there was an instantaneous drop in heart rate (up to 15 beats min–1) as the heat source was switched off, and this drop in heart rate coincided with either a drop in β-adrenergic tone or an increase in cholinergic tone. Rates of heating were significantly faster during the cholinergic blockade, and least with a combined cholinergic and β-adrenergic blockade. The results showed that cholinergic and β-adrenergic systems are not the only control mechanisms acting on the heart during heating and cooling, but they do have a significant effect on heart rate and on rates of heating and cooling.


2020 ◽  
Author(s):  
Shin Yoo ◽  
Markus Rottmann ◽  
Jason Ng ◽  
David Johnson ◽  
Bassel Shanab ◽  
...  

ABSTRACTBackgroundAlthough atrial electrograms (EGMs) are thought to reflect pathophysiological substrate for atrial fibrillation (AF), it is not known which electrograms are suitable targets during AF ablation. We hypothesized that electrogram morphology recurrence (EMR) better reflects arrhythmogenic AF substrate than traditional frequency and complexity measures of AF. In a canine rapid atrial pacing (RAP) model of AF, we assessed the relationship between EMR and traditional AF electrogram measures, rotational activity in the atria, fibrosis, myofiber orientation and parasympathetic innervation.MethodsPersistent AF was induced in 13 dogs by RAP for 6-8 weeks. High-density epicardial mapping (117 electrodes) was performed in six atrial sub-regions. EMR measures Recurrence percentage (Rec%) and cycle length of the most frequent electrogram morphology (CLR), Fractionated Interval (FI), Organization Index (OI), Dominant Frequency (DF) and Shannon’s Entropy (ShEn) were analyzed before and after atropine administration. Myocyte fiber orientation, amount of fibrosis and spatial distribution of parasympathetic nerve fibers were quantified.ResultsRec% was greatest in the appendages, and CLR was lowest in the posterior left atrium. Rec%/CLR correlated with FI, OI and the complexity measure ShEn, but not with DF. All electrogram measures were poorly correlated with fibrosis and myofiber anisotropy. Rec% correlated closely with stability of rotational activity. Unlike other measures, Rec% correlated closely with spatial heterogeneity of parasympathetic nerve fibers; this was reflected in CLR response to atropine.ConclusionEMR correlates closely with stability of rotational activity and with the pattern of atrial parasympathetic innervation. CLR may therefore be a viable therapeutic target in persistent AF.


1992 ◽  
Vol 82 (2) ◽  
pp. 139-145 ◽  
Author(s):  
S. J. Cross ◽  
M. R. Cowie ◽  
J. M. Rawles

1. In six healthy subjects the amplitude and phase of respiratory sinus arrhythmia were determined at five different respiratory cycle lengths ranging from 3 to 9.5 s. 2. At each respiratory cycle length the carotid baroreceptor-heart rate reflex response was determined by cyclical neck suction at −40 mmHg at five different cycle lengths covering the same range of 3–9.5 s. 3. The application of cyclical neck suction increased the amplitude of respiratory sinus arrhythmia in all but the longest respiratory cycle lengths. 4. With increasing respiratory cycle length the amplitude of sinus arrhythmia increased, and R-R intervals were at their longest at an earlier phase of the respiratory cycle. Similarly, with increasing suction cycle length the amplitude of the cardiac interval response increased and the phase angle decreased. 5. The cardiac interval responses to respiration and to neck suction at different frequencies were independent of each other, the heart rate at any moment resulting from the algebraic summation of the two responses.


2000 ◽  
Vol 279 (3) ◽  
pp. H1000-H1006 ◽  
Author(s):  
John G. Lainchbury ◽  
Donna M. Meyer ◽  
Michihisa Jougasaki ◽  
John C. Burnett ◽  
Margaret M. Redfield

Myocardial actions of the vasodilator peptide adrenomedullin (ADM) in the intact animal are unknown. Negative and positive inotropic actions have been reported in ex vivo experiments. Myocardial and load-altering actions of ADM in dogs before and after development of heart failure were studied. With controlled heart rate (atrial pacing) and after β-blockade, ADM was administered to five normal dogs in doses of 20 ng · kg−1 · min−1 iv, 100 ng · kg−1 · min−1 iv, and 200 ng · kg−1 · min−1 into the left ventricle (LV). LV peak systolic pressure and end-systolic volume decreased with each dose of ADM. End-systolic pressure decreased with the two higher doses. At the highest dose, arterial elastance and the time constant of LV isovolumic relaxation (τ) decreased, and LV end-systolic elastance ( E es) increased. LV end-diastolic pressure and volume were unchanged. In five additional normal dogs receiving only the highest dose of ADM (200 ng · kg−1 · min−1 intra-LV), to control for increased heart rate and sympathetic activation observed with the cumulative infusion, ADM produced arterial vasodilation but no change in E es or τ. In four dogs with pacing-induced heart failure, ADM (200 ng · kg−1 · min−1 intra-LV) was without effect on τ, E es, and systolic or diastolic pressure and volume. In vivo, ADM appears to be a selective arterial dilator without inotropic or lusitropic effects. The vasodilatory actions are attenuated in heart failure.


1991 ◽  
Vol 260 (3) ◽  
pp. H985-H988 ◽  
Author(s):  
D. C. Randall ◽  
D. R. Brown ◽  
R. M. Raisch ◽  
J. D. Yingling ◽  
W. C. Randall

The purpose of this study was to quantify the relative roles of the canine cardiac parasympathetic and sympathetic nerves in controlling the distribution of power within the heart rate (HR) power spectrum using a highly selective surgical technique to parasympathectomize the SA node. DAta were recorded in awake dogs (n = 6) before and after the selective denervation; the animals were isolated from human contact and their behavior carefully monitored during the measurements. The average amplitude in the high-frequency (approximately 0.32 Hz) peak in the HR power spectrum decreased from a predenervation control of 2.68 +/- 1.54 (mean +/- SD, arbitrary units) to 0.07 +/- 0.06 (P less than 0.05). Corresponding resting HR increased from 80 +/- 9 to 106 +/- 16 beats/min (P less than 0.05). The low-frequency peak (approximately 0.02 Hz) also decreased from a control of 2.45 +/- 1.18 to a postparasympathectomy value of 1.25 +/- 0.92 (P less than 0.05). beta-Adrenergic blockade (propranolol, 1 mg/kg) further decreased the latter peak to 0.59 +/- 0.52 (P less than 0.05). These data directly demonstrate that the high-frequency peak of the HR power spectrum 1) results from parasympathetic control of SA nodal automaticity, while 2) the low-frequency peak reflects activity in both divisions of the autonomic nervous system.


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