Altered nicotinic sensitivity of AV node in surgically denervated canine hearts

1983 ◽  
Vol 245 (1) ◽  
pp. H27-H32
Author(s):  
D. V. Priola ◽  
M. B. Curtis ◽  
C. Anagnostelis ◽  
E. Martinez
Keyword(s):  
Fold Increase ◽  
Conduction Time ◽  
Mediating Effects ◽  
Extrinsic Denervation ◽  
Av Node ◽  
Intraventricular Conduction ◽  
Denervation Supersensitivity ◽  
Muscarinic Stimulation ◽  
Intrinsic Cardiac Nerves ◽  
Cardiac Nerves

The responses of normal and cardiac-denervated (DNV) dogs to acetylcholine (ACh) and nicotine (NIC) were examined to determine if the intrinsic cardiac nerves (ICN) that modulate electrical conduction display denervation supersensitivity. Control (n = 18) and DNV (n = 18) animals were placed on cardiopulmonary bypass. Recording of intra-atrial (P-A), intraventricular (H-V), and atrioventricular (AV) nodal (A-H) conduction times were made from the region of the His bundle. ACh (0.1-10 micrograms) was used to produce muscarinic stimulation, whereas NIC (0.1-400 micrograms) was employed to stimulate the ICN. All drugs were administered intracoronary. No supersensitivity to either ACh or NIC was seen in the data from the P-A or H-V intervals of the His electrogram in the DNV animals. However, this group displayed approximately a 10-fold increase in the negative dromotropic effect of NIC on the AV node compared with control. No significant change in muscarinic sensitivity of the AV node was observed in the DNV animals. We conclude that 1) no denervation supersensitivity of the ICN mediating effects on intra-atrial and intraventricular conduction occurs; 2) the AV node itself does not show muscarinic supersensitivity following extrinsic denervation; 3) the ICN do display denervation supersensitivity as shown by a 10-fold increase in the effects of NIC on AV nodal conduction time.

Intrinsic neural regulation of the heart in the chronic, conscious dog

1998 ◽  
Vol 274 (6) ◽  
pp. H2074-H2084 ◽  
Author(s):  
Donald V. Priola ◽  
Xiaoling Cao ◽  
Constantine Anagnostelis ◽  
Eberhard Bassenge
Keyword(s):  
Left Atrial ◽  
Cardiac Performance ◽  
Conduction Time ◽  
Direct Effects ◽  
Av Node ◽  
Cardiac Denervation ◽  
Conscious Dog ◽  
Av Conduction ◽  
Intrinsic Cardiac Nerves ◽  
Cardiac Nerves

The present experiments were performed to examine the capability of the intrinsic cardiac nerves (ICN) to modify cardiac performance in the resting chronic, conscious dog. Control and cardiac-denervated dogs were instrumented for recording of left atrial (LA) and ventricular (LV) contractility, heart rate, and atrioventricular (AV) conduction time. Acetylcholine (ACh) and nicotine (Nic) were administered via an indwelling coronary artery catheter. Limited distribution from the injection site only allowed access to the LA, LV, and AV node. Both β-blockade with timolol and cardiac denervation were used to separate direct effects of ICN stimulation from indirect (e.g., reflex) effects. ACh produced the expected negative inotropic and dromotropic changes. ICN stimulation with Nic caused large decreases in LA contractility along with depression of AV conduction but only trivial effects on the LV. We concluded that the ICN has limited effects on cardiac performance in the resting animal under minimal sympathetic drive. It is likely, however, that the ICN is capable of significantly depressing cardiac function under conditions of elevated sympathetic tone as would be encountered in exercise.

Integration of heart rate and sympathetic neural effects on AV conduction

1988 ◽  
Vol 254 (4) ◽  
pp. H651-H657
Author(s):  
J. M. Loeb ◽  
J. M. deTarnowsky
Keyword(s):  
Heart Rate ◽  
Sympathetic Activity ◽  
Sinoatrial Node ◽  
Conduction Time ◽  
Atrial Pacing ◽  
Sympathetic Stimulation ◽  
Sympathetic Activation ◽  
Direct Effects ◽  
Av Node ◽  
Av Conduction

Sympathetic activation increases heart rate (HR) and reduces atrioventricular interval (AVI), whereas atrial pacing alone increases AVI. We sought to differentiate the direct effects of sympathetic activation on atrioventricular (AV) conduction time from the indirect changes associated with concurrent alterations in HR. We recorded electrocardiograms, blood pressure (BP), and intracardiac electrograms from chloralose-anesthetized autonomically decentralized dogs. Beat-by-beat HR and AVI data were collected continuously. Sympathetic stimulation (0.25-2.5 Hz; mean 0.81 Hz) resulted in a HR change of +60 beats/min after 60 s. This tachycardia was associated with a mean decrease in AVI of 22 ms. Computer-driven atrial pacing to reproduce the HR associated with control sympathetic stimulation caused a mean AVI increase of 10 ms. Propranolol (200 micrograms) was then administered via the sinoatrial node artery and sympathetic stimulation repeated. Although HR remained constant, AVI decreased by 14.8 ms. The AVIs associated with an identical HR achieved by two different mechanisms (sympathetic stimulation and atrial pacing) were significantly different. Although removal of the contribution of sympathetically induced HR changes on AV conduction might be expected to result in potentiation of neural effects at the AV node, none was evident. Thus sympathetic activity restricted to the AV node is less effective in influencing AV conduction than the response that occurs when HR changes occur concurrently. Therefore, the opposing actions of HR and sympathetic tone on AV conduction may not be predicted by a simple linear relationship.

scholarly journals Prognostic Implications of ‘Paced’ and ‘Native’ QRS Durations Following Cardiac Resynchronization Therapy

2016 ◽  
Vol 02 (01) ◽  
pp. 30
Author(s):  
Oguz Karaca ◽  
Keyword(s):  
Cardiac Resynchronization Therapy ◽  
Response To Therapy ◽  
Cardiac Resynchronization ◽  
Current Evidence ◽  
Conduction Time ◽  
Resynchronization Therapy ◽  
Intraventricular Conduction ◽  
Surface Ecg ◽  
Future Outcomes ◽  
Electrocardiographic Parameters

Current evidence strongly suggests that the extent of electrical dyssynchrony within the left ventricle is determined by the delayed intraventricular conduction time reflected by a prolonged QRS duration (QRSd) on the surface (ECG). However, in cardiac resynchronization therapy (CRT) follow-up algorithms, the QRSd on the post-operative ECG has been relatively less frequently addressed, although the baseline QRSd is accepted as an essential ‘pre-operative’ marker for patient selection and prediction of response to therapy. In this review, we discuss the clinical impact of post-implantation electrocardiographic parameters, such as the ‘paced’ QRSd and ‘native’ QRSd (assessed when the device is temporarily switched off) on the efficacy of therapy and on prediction of future outcomes after CRT.

Source of intrinsic innervation of canine ventricles: a functional study

1987 ◽  
Vol 252 (3) ◽  
pp. H638-H644 ◽  
Author(s):  
T. M. Blomquist ◽  
D. V. Priola ◽  
A. M. Romero
Keyword(s):  
Cardiopulmonary Bypass ◽  
Ganglion Cells ◽  
Functional Study ◽  
Beta Blockade ◽  
Parasympathetic Innervation ◽  
Intrinsic Innervation ◽  
Series Of Experiments ◽  
Intrinsic Cardiac Nerves ◽  
Cardiac Nerves

Recently it has been suggested that the parasympathetic innervation of the ventricles is by way of postganglionic axones that emanate from ganglion cells in the atria, reaching the ventricles by traversing the atrioventricular (AV) groove. We designed a series of experiments to test this hypothesis. Phenol (89%) was applied to the AV groove and surrounding 5 mm of epicardium in 21 dogs on cardiopulmonary bypass. The effects of intracoronary acetylcholine (ACh; 1-5 micrograms) and intracoronary nicotine (NIC; 25–100 micrograms) on cardiac isovolumic pressures were evaluated after beta-blockade. In another series of experiments, eight dogs were exposed to phenol in the same way and allowed to recover for 7–10 days. Atrial and ventricular responses to NIC were unaffected by phenol application to the AV groove in the acute animals when compared with application of saline alone. However, in the chronic animals, pretreatment with phenol 7–10 days previously reduced the ventricular responses to NIC by 70% while leaving the atrial responses intact. These data indicate that the intrinsic cardiac nerves (ICN) of the canine ventricles consist primarily of postganglionic parasympathetic axones which arise from supraventricular ganglia and cross the AV groove.

Effect of anomalous pathway location on rate of canine experimental A-V reentrant tachycardia

1977 ◽  
Vol 233 (1) ◽  
pp. H44-H49
Author(s):  
S. Teague ◽  
P. Denes ◽  
F. Amat-y-Leon ◽  
K. M. Rosen
Keyword(s):  
Cycle Length ◽  
Electronic Circuit ◽  
The Other ◽  
Conduction Time ◽  
Reentrant Tachycardia ◽  
Intraventricular Conduction ◽  
Atrial Refractoriness ◽  
The Relationship ◽  
Atrial Stimulation ◽  
Anterior Posterior

The effect of anomalous pathway (AP) location and conduction time on the cycle length (CL) and sustainability of paroxysmal A-V reentrant tachycardia was studied in 15 dogs, using an anomalous pathway simulator (APS). The APS was a programmable digital electronic circuit with ability for unidirectional conduction, ventricular sensing, adjustable delay, and atrial stimulation. Contiguous pairs of ventricular sensing electrodes were placed along the A-V ring in each dog at the following sites: anterior, posterior, and lateral right (AR, PR, and LR) and anterior, posterior, and lateral left (AL, PL, and LL) and septal (S). There were significant differences in the CL of tachycardias among the tested sites (P less than 0.01). The CL of tachycardias from the LL site was significantly longer and from the PR site significantly shorter than that from the other sites (P less than 0.05). These differences in CL of tachycardias in relation to the AP location were explicable in terms of corresponding variation in conduction times of the various components of the tachycardia circuit (e.g., intra-atrial, A-V nodal, intraventricular conduction times). The differences in magnitude of the CL of tachycardias, although significant, were small. It was also found that all sites allowed maintenance of tachycardias up to an AP conduction time of 10 ms. In 27% of experiments, atrial refractoriness prevented sustained tachycardias at pathway delays of 1 ms. The relationship between AP conduction time and CL of tachycardias was exponential.

Modulation of AV nodal and Hisian conduction by changes in extracellular space

1999 ◽  
Vol 276 (3) ◽  
pp. H953-H960
Author(s):  
Keith G. Lurie ◽  
Atsushi Sugiyama ◽  
Scott McKnite ◽  
Paul Coffeen ◽  
Keitaro Hashimoto ◽  
...  
Keyword(s):  
Extracellular Space ◽  
Left Ventricular ◽  
Conduction Time ◽  
Av Node ◽  
Total Blood ◽  
His Bundle ◽  
Induced Changes ◽  
Total Blood Flow ◽  
Dose Dependent Increase ◽  
Dose Dependent

Previous studies have demonstrated that the extracellular space (ECS) component of the atrioventricular (AV) node and His bundle region is larger than the ECS in adjacent contractile myocardium. The potential physiological significance of this observation was examined in a canine blood-perfused AV nodal preparation. Mannitol, an ECS osmotic expander, was infused directly into either the AV node or His bundle region. This resulted in a significant dose-dependent increase in the AV nodal or His-ventricular conduction time and in the AV nodal effective refractory period. Mannitol infusion eventually resulted in Wenckebach block ( n = 6), which reversed with mannitol washout. The ratio of AV nodal to left ventricular ECS in tissue frozen immediately on the development of heart block ( n = 8) was significantly higher in the region of block (4.53 ± 0.61) compared with that in control preparations (2.23 ± 0.35, n = 6, P < 0.01) and donor dog hearts (2.45 ± 0.18, n = 11, P < 0.01) not exposed to mannitol. With lower mannitol rates (10% of total blood flow), AV nodal conduction times increased by 5–10% and the AV node became supersensitive to adenosine, acetylcholine, and carbachol, but not to norepinephrine. We conclude that mannitol-induced changes in AV node and His bundle ECS markedly alter conduction system electrophysiology and the sensitivity of conductive tissues to purinergic and cholinergic agonists.

Separate parasympathetic control of heart rate and atrioventricular conduction of dogs

1990 ◽  
Vol 259 (2) ◽  
pp. H536-H542 ◽  
Author(s):  
D. W. Wallick ◽  
P. J. Martin
Keyword(s):  
Vena Cava ◽  
Atrioventricular Conduction ◽  
Conduction Time ◽  
Fat Pad ◽  
Av Node ◽  
Parasympathetic Ganglia ◽  
Anesthetized Dogs ◽  
Parasympathetic Control ◽  
The Right ◽  
Electrical Stimuli

In open-chest, autonomically decentralized, anesthetized dogs, a brief burst of electrical stimuli was delivered at various time delays to the right pulmonary vein (RPV) fat pad. This fat pad contains parasympathetic ganglia that innervate the sinoatrial (SA) node. Each burst elicited a bimodal increase in the cardiac cycle length (CCL) without eliciting a significant change in atrioventricular conduction time (AVCT). A similar burst was applied to the inferior vena cava-inferior left atrial fat pad. This fat pad contains nerves that innervate the AV node. This latter stimulation elicited a bimodal increase in AVCT without eliciting any change in the CCL. When the cervical vagi were stimulated in a similar manner, a bimodal increase in the CCL was elicited that was similar to the response we observed when the RPV fat pad was stimulated. In contrast, the dromotropic response was quite variable. In conclusion, we could, for the most part, elicit selective parasympathetic control of either the SA or the AV node, respectively.

Intraventricular conduction time in patients with bundle branch block

1973 ◽  
Vol 6 (3) ◽  
pp. 181-192 ◽  
Author(s):  
Prem K. Gupta ◽  
Kul D. Chadda ◽  
Edgar Lichstein ◽  
Ho-Mau Liu ◽  
Majeed Sayeed
Keyword(s):  
Conduction Time ◽  
Bundle Branch Block ◽  
Intraventricular Conduction

scholarly journals Effects of Volatile Anesthetics on Atrial and AV Nodal Electrophysiological Properties in Guinea Pig Isolated Perfused Heart 

1998 ◽  
Vol 89 (2) ◽  
pp. 434-442 ◽  
Author(s):  
Pekka M. J. Raatikainen ◽  
Mark F. Trankina ◽  
Timothy E. Morey ◽  
Donn M. Dennis
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Action Potential Duration ◽  
Volatile Anesthetics ◽  
Monophasic Action Potential ◽  
Computer Assisted ◽  
Conduction Time ◽  
Av Node ◽  
Refractory Periods ◽  
Supraventricular Tachycardias

Background Knowledge of the anesthetic effects on atrial and atrioventricular (AV) nodal electrophysiologic properties is fundamental to understand the modulatory role of anesthetics on the pathogenesis of supraventricular tachycardias, and to individualize the perioperative management of patients with supraventricular tachycardias or AV nodal conduction disturbances. Therefore the authors studied the effects of three commonly used volatile anesthetics on the electrophysiologic properties of the atrium and AV node. Methods The concentration-dependent electrophysiologic effects of halothane, isoflurane, and desflurane (0-2 minimum alveolar concentration [MAC]) were studied in guinea pig Langendorff-perfused hearts fit with instruments to simultaneously measure atrial and AV nodal conduction times and atrial monophasic action potential duration. Atrial and AV nodal effective refractory periods were measured simultaneously using a computer-assisted premature stimulation protocol. The concentrations of anesthetics in the gas phase were monitored by an infrared gas analyzer. Results Volatile anesthetics caused markedly different concentration-dependent effects on atrial conduction, repolarization, and refractoriness, and on AV nodal function. At equianesthetic concentrations, halothane depressed atrial conduction the most, whereas desflurane caused the greatest shortening of atrial monophasic action potential duration. Halothane had no significant effect on atrial refractoriness, whereas at 2 MAC desflurane significantly shortened and isoflurane significantly prolonged atrial effective refractory periods by 18.1+/-13.5% and 13.2+/-14.7%, respectively. On an equi-MAC basis, the rank order of potency for the anesthetics to prolong AV nodal conduction time and AV nodal ERP was halothane &gt; desflurane &gt; isoflurane. Conclusion The different electrophysiologic effects of volatile anesthetics in the atrium and AV node suggest that these agents may modulate atrial dysrhythmogenesis in distinctly different ways.

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