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.

Inotropic, chronotropic, and dromotropic effects mediated via parasympathetic ganglia in the dog heart

2000 ◽  
Vol 279 (3) ◽  
pp. H1201-H1207 ◽  
Author(s):  
Masato Tsuboi ◽  
Yasuyuki Furukawa ◽  
Koichi Nakajima ◽  
Fumio Kurogouchi ◽  
Shigetoshi Chiba
Keyword(s):  
Superior Vena ◽  
Vena Cava ◽  
Contractile Force ◽  
Right Atrial ◽  
Fat Pad ◽  
Parasympathetic Ganglia ◽  
Dog Heart ◽  
Parasympathetic Nerves ◽  
Av Conduction ◽  
Stimulation Of

Some parasympathetic ganglionic cells are located in the epicardial fat pad between the medial superior vena cava and the aortic root (SVC-Ao fat pad) of the dog. We investigated whether the ganglionic cells in the SVC-Ao fat pad control the right atrial contractile force, sinus cycle length (SCL), and atrioventricular (AV) conduction in the autonomically decentralized heart of the anesthetized dog. Stimulation of both sides of the cervical vagal complexes (CVS) decreased right atrial contractile force, increased SCL, and prolonged AV interval. Stimulation of the rate-related parasympathetic nerves to the sinoatrial (SA) node (SAPS) increased SCL and decreased atrial contractile force. Stimulation of the AV conduction-related parasympathetic nerves to the AV node prolonged AV interval. Trimethaphan, a ganglionic nicotinic receptor blocker, injected into the SVC-Ao fat pad attenuated the negative inotropic, chronotropic, and dromotropic responses to CVS by 33∼37%. On the other hand, lidocaine, a sodium channel blocker, injected into the SVC-Ao fat pad almost totally inhibited the inotropic and chronotropic responses to CVS and partly inhibited the dromotropic one. Lidocaine or trimethaphan injected into the SAPS locus abolished the inotropic responses to SAPS, but it partly attenuated those to CVS, although these treatments abolished the chronotropic responses to SAPS or CVS. These results suggest that parasympathetic ganglionic cells in the SVC-Ao fat pad, differing from those in SA and AV fat pads, nonselectively control the atrial contractile force, SCL, and AV conduction partially in the dog heart.

Effect of disopyramide and disobutamide on conduction in perfused rabbit hearts

1981 ◽  
Vol 59 (11) ◽  
pp. 1192-1195
Author(s):  
Peter E. Dresel ◽  
Keith D. Cameron
Keyword(s):  
Antiarrhythmic Agent ◽  
Conduction System ◽  
Atrioventricular Conduction ◽  
Cardiac Conduction ◽  
Conduction Time ◽  
Related Effect ◽  
Av Node ◽  
His Bundle ◽  
Time Changes ◽  
His Bundle Recording

The effects of disopyramide (DP) and a new antiarrhythmic agent, disobutamide (DB) on cardiac conduction were studied using His bundle recording from modified rabbit Langendorff preparations electrically driven at 3 and 4 Hz. Both disopyramide (4–16 μg/mL) and disobutamide (1–30 μg/ml) slowed conduction throughout the atrioventricular conduction system, i.e., SA, AH, and HV intervals were increased in a dose-related manner. Conversion of the conduction time changes to percent changes indicates that disobutamide has a relatively equal effect on each part of the system whereas disopyramide exhibited significantly less effect on AV nodal conduction. Slowing of conduction in the AV node by DP was clearly related to rate. Changes in SA and HV intervals were rate related to a lesser degree. No such rate-related effect was evident with disobutamide. Block of atrial conduction occurred in two out of six hearts when the rate was increased at 8 μg/mL of DP and in three additional hearts at 16 μg/mL. This was interpreted to indicate a change in atrial excitability such that 2 × threshold currents no longer excited the tissues. This was not observed at any concentration of DB.

Epicardial sites for vagal mediation of sinoatrial function

1992 ◽  
Vol 262 (5) ◽  
pp. H1401-H1406 ◽  
Author(s):  
J. D. Mick ◽  
R. D. Wurster ◽  
M. Duff ◽  
M. Weber ◽  
W. C. Randall ◽  
...  
Keyword(s):  
Discharge Rate ◽  
Vena Cava ◽  
Electrical Current ◽  
Retrograde Transport ◽  
Right Atrial ◽  
Bipolar Electrode ◽  
Fat Pad ◽  
Neuronal Marker ◽  
Parasympathetic Ganglia ◽  
Series Of Experiments

The posterior atrial fat pad (PAFP) has been described as the probable anatomic location of parasympathetic ganglia mediating sinoatrial (SAN) and atrioventricular nodal function in the mammalian heart. This contrasts with recent localizations of such control elements in the pulmonary vein fat pad (PVFP) and in fatty tissues overlying the junction of inferior vena cava-inferior left atrium (IVC-ILA), respectively. Short bursts (5-8 pulses/burst, 3 bursts/train) of electrical current (1-16 Hz, 400 ms, 1-5 mA) applied directly to the ventral right atrial epicardium via a concentric bipolar electrode (separation 0.3-0.6 mm) during the atrial muscle refractory period, activated subepicardial postganglionic pathways from PVFP and entering the SAN; identical stimulation of dorsal right atrial epicardium between PAFP and SAN excited few or no fiber pathways controlling SAN discharge rate or patterns. In a second series of experiments, injection of a neuronal marker (Fast Blue) into and around SAN, with time (5-10 days) allowed for retrograde transport, resulted in staining of many soma in PVFP but none in IVC-ILA or PAFP. These data strongly affirm the primary, and perhaps exclusive, localization of ganglia that mediate parasympathetic regulation of SAN function in PVFP of the dog's heart, with little or no such participation by ganglia within PAFP or IVC-ILA.

Arrhythmias

2014 ◽  
pp. 851-859
Author(s):  
Murali Chiravuri ◽  
Thomas M. Tadros ◽  
Usha B. Tedrow
Keyword(s):  
Coronary Artery ◽  
Right Coronary Artery ◽  
Superior Vena ◽  
Vena Cava ◽  
Av Node ◽  
Circumflex Artery ◽  
Left Circumflex Artery ◽  
Sa Node ◽  
Bundle Of His ◽  
The Right

In the normal heart the sinoatrial (SA) node serves as the principal pacemaker and determines the heart rate. The SA node consists of groups of pacemaker cells marked by their ability to spontaneously depolarize and are located at the junction of the right atrium and the superior vena cava. The blood supply to the SA node is variable with the sinus nodal artery arising from the right coronary artery in 60% percent of cases and from the left circumflex artery in 40% of cases. Following depolarization of the SA nodal cells, the signal traverses the atrium before arriving at the atrioventricular (AV) node. The AV node is marked by its ability to delay impulse propagation, which allows for coordinated contraction of the atria and ventricles. The AV nodal artery arises from the right coronary artery in 90% of cases and from the left circumflex artery in 10% of cases. After exiting the AV node, the impulse is transmitted through the bundle of His, the right and left bundle branches, and ultimately exits the terminal Purkinje fibers of the conduction system into the myocardium near the apex of the heart.

Effect of phasic vagal stimulation and atrial pacing site on atrioventricular conduction time

1997 ◽  
Vol 272 (5) ◽  
pp. H2289-H2298 ◽  
Author(s):  
D. A. Igel ◽  
D. W. Wallick ◽  
P. J. Martin ◽  
M. N. Levy
Keyword(s):  
Coronary Sinus ◽  
Cycle Length ◽  
Vagal Stimulation ◽  
Interatrial Septum ◽  
Conduction Time ◽  
Atrial Pacing ◽  
Av Conduction ◽  
Recovery Times ◽  
Anesthetized Dogs ◽  
The Right

We tested the hypothesis that the effect of phasic vagal stimulation on atrioventricular (AV) conduction time is affected by the site of atrial pacing in anesthetized dogs. We paced the right atrium at a constant cycle length from the interatrial septum (IAS), superior coronary sinus (SCS), or inferior coronary sinus (ICS) regions, and we evaluated the time-dependent effects of vagal stimulation on AV conduction at each pacing site. When we stimulated the vagi at stimulus (St)-A phases greater than 136 +/- 40 ms and less than the phase that blocked AV conduction (182 +/- 70 ms), IAS pacing prolonged A-V intervals by 8.6 +/- 8.2 ms more than ICS pacing. A change in pacing site affected the A-V intervals by up to 30 ms when we stimulated the vagus at those times that caused the A-V intervals to prolong maximally. Furthermore, the effect of atrial pacing site on A-V intervals was modulated by AV nodal recovery times during the second or third cycles after the vagal stimulus.

scholarly journals AN EXPERIMENTAL STUDY OF DIATHERMY

1927 ◽  
Vol 46 (4) ◽  
pp. 595-600 ◽  
Author(s):  
Carl A. L. Binger ◽  
Ronald V. Christie
Keyword(s):  
High Frequency ◽  
Inferior Vena ◽  
Vena Cava ◽  
Hepatic Veins ◽  
Left Heart ◽  
Right Heart ◽  
Anesthetized Dogs ◽  
Heart Blood ◽  
The Right ◽  
Thermo Couple

1. A method of measuring intravascular temperatures in anesthetized dogs has been described. 2. The temperature in the abdominal aorta is uniform throughout, and varies only with the systemic temperature. 3. The temperature in the inferior vena cava rises as the thermo-couple approaches the heart, reaching its maximum at about the level of the hepatic veins. Between the hepatic veins and the right chambers of the heart there is no further elevation in venous temperature. 4. The temperature of the right heart blood normally exceeds that of the left heart blood by 0.05–0.2°C. 5. During the application of high frequency currents to the thorax, this relationship is reversed. 6. This indicates that the lungs are being heated but that the blood passing through the pulmonary vessels is removing the heat at approximately the rate of production.

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

1986 ◽  
Vol 251 (5) ◽  
pp. H920-H925 ◽  
Author(s):  
J. Billette ◽  
J. P. Gossard ◽  
L. Lepanto ◽  
R. Cartier
Keyword(s):  
Steady State ◽  
Atrioventricular Node ◽  
Sequential Patterns ◽  
Functional Domain ◽  
Conduction Time ◽  
Atrial Pacing ◽  
Av Node ◽  
Anesthetized Dogs ◽  
Atrioventricular Nodal Conduction ◽  
Transient And Steady State

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.

Prevention of diminished parasympathetic control of the heart in experimental heart failure

2004 ◽  
Vol 287 (4) ◽  
pp. H1780-H1785 ◽  
Author(s):  
Steve Bibevski ◽  
Mark E. Dunlap
Keyword(s):  
Heart Failure ◽  
Synaptic Transmission ◽  
Sinus Node ◽  
Parasympathetic Ganglia ◽  
Sinus Cycle Length ◽  
Parasympathetic Control ◽  
The Right ◽  
Parasympathetic Function ◽  
Nicotinic Agonist

Decreased synaptic transmission in parasympathetic ganglia contributes to abnormal parasympathetic function in heart failure (HF). Because nicotinic ACh receptors (nAChR) mediate synaptic transmission at the ganglion and upregulate in response to chronic exposure to agonist in vitro, we tested the hypothesis that repeated exposures of ganglionic neurons to a nAChR agonist can prevent a loss of parasympathetic control in HF. Two sets of experiments were performed. In set 1, unpaced control dogs and dogs undergoing pacing-induced HF were treated with a repeated intravenous nicotinic agonist during the development of HF. Under conditions of sympathetic blockade, R-R responses to a bolus injection of 200 μg 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP; nicotinic agonist) were found to be increased five times over the untreated group after 6 wk. In experimental set 2, dogs treated with weekly DMPP injections and in HF were anesthetized and underwent electrical stimulation of the right vagus nerve, which showed sinus cycle length responses >10 times that of controls ( P < 0.05). Complete ganglionic blockade with hexamethonium abolished all responses, confirming that synaptic transmission was mediated entirely by nAChRs in both controls and HF. Despite decreased ganglionic function leading to reduced parasympathetic control of the heart in HF, repeated exposure with a nicotinic agonist during the development of HF results in not only preserved but also supranormal effects of parasympathetic stimulation on the sinus node.

Role of mixed venous blood Pco2 in respiratory control

1961 ◽  
Vol 16 (6) ◽  
pp. 1029-1033 ◽  
Author(s):  
Gerd J. A. Cropp ◽  
Julius H. Comroe
Keyword(s):  
Venous Blood ◽  
Vena Cava ◽  
Respiratory Control ◽  
Minute Volume ◽  
Regulation Of Respiration ◽  
Mixed Venous Blood ◽  
Physiological Regulation ◽  
Anesthetized Dogs ◽  
The Right ◽  
Mixed Venous

The Pco2 of mixed venous blood has been increased abruptly by 5—49 mm Hg, without altering the volume or pressure of blood returning to the right ventricle, by infusion of blood with 550—700 mm Hg Pco2 into the right atrium, and simultaneous withdrawal of equal volumes of blood from the inferior vena cava. Twenty-five such blood exchanges in four anesthetized cats, four anesthetized dogs, and three unanesthetized dogs failed, with one exception, to increase respiratory frequency or tidal volume if PaCOCO2 remained constant; respiration increased only when PaCOCO2 rose. Correlation of ventilatory minute volume with PvCOCO2 was poor ( r = 0.296; P > 0.1) but was good with PaCOCO2 ( r = 0.608; P < 0.001). Experiments on the innervated and denervated carotid body (dog) demonstrated that chemoreceptors can respond rapidly (0.5 sec) to changes in PaOO2 or PaCOCO2. The absence of demonstrable ventilatory response to increased PvCOCO2 over periods of 0.5–3.0 min in animals in whom increments in PaCOCO2 led promptly to increased ventilation indicates that there are no CO2 receptors in the precapillary pulmonary circulation of importance in the physiological regulation of respiration. Submitted on May 25, 1961

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