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.

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.

Cardiorenal effects of lidocaine and procaine amide in the conscious dog

1975 ◽  
Vol 228 (5) ◽  
pp. 1440-1445 ◽  
Author(s):  
WJ Mandel ◽  
MM Laks ◽  
AI Arieff ◽  
K Obayashi ◽  
H Hayakawa ◽  
...  
Keyword(s):  
Renal Function ◽  
Cardiac Conduction ◽  
Right Atrial ◽  
Acute Administration ◽  
Conduction Time ◽  
Conscious Dog ◽  
Av Conduction ◽  
Renal Flow ◽  
The Right ◽  
Procaine Amide

Simultaneous measurements of hemodynamics, arterioventricular (AV) conduction, and renal functioner were obtained in conscious dogs. Catheters were implanted for the long-term measurement of central aortic, right ventricular, and pulmonary artery pressure. AV conduction was assessed following surgical implantation of multipolar electrode plaques in the area of the bundle of His, as well as on the epicardium of the right and left atria and ventricles. Renal function was assessed utilizing standard techniques. Following control measurements, lidocaine, 1 mg/kg, or procaine amide, 10 mg/kg, was administered intravenously. Subsequently, serial measurements were obtained for a 90-min period. No significant changes in hemodynamics were observed following either drug. Procaine amide produced a significant increase in heart rate and a minimal increase in QRS duration associated with a decrease in low right atrial to His bundle conduction time. However, no significant changes in cardiac conduction were observed after lidocaine administration. Renal function was unaffected by lidocaine but significantly depressed by procaine amide, as demonstrated by a decrease in GFR and effective renal flow. In summary, acute administration of procaine amide significantly alters renal function in the conscious dog with minimal effects on AV conduction and hemodynamics.

Differential effect of verapamil isomers on sinus node and AV junctional region

1983 ◽  
Vol 244 (1) ◽  
pp. H80-H88
Author(s):  
H. O. Gloor ◽  
F. Urthaler
Keyword(s):  
Sinus Rhythm ◽  
Sinus Node ◽  
Conduction Time ◽  
Av Node ◽  
Junctional Rhythm ◽  
His Bundle ◽  
Sinus Node Artery ◽  
Rate Dependent ◽  
Av Conduction ◽  
Differential Responsiveness

The l- and d-isomers of verapamil were selectively perfused into the sinus node artery and atrioventricular (AV) node artery of 48 dogs. Injection of l-verapamil into the sinus node artery during sinus rhythm and into the AV node artery during AV junctional rhythm depresses both sinus rhythm and AV junctional rhythm significantly more than does the d-isomer. l-Verapamil is three to four times more powerful than d-verapamil. Injection of the isomers into the AV node artery during sinus rhythm rapidly impairs AV conduction. Increments in conduction time are measured exclusively at the level of the A-H interval of the His bundle electrogram, and l-verapamil is six times more powerful than d-verapamil. Neither d- nor l-verapamil in concentrations that exert a profound negative chronotropic effect or cause AV block, has any significant effect on transatrial or His bundle conduction. Thus these concentrations of d-verapamil have little or no significant effect on the fast sodium channel, but both verapamil isomers affect the slow channel. The main difference in action between l- and d-verapamil appears to be only quantitative in nature. The sinus node is significantly more sensitive to the negative chronotropic action of verapamil than is the AV junctional pacemaker, and this differential responsiveness appears to be related to the different intrinsic rates of the two pacemakers. During sinus rhythm (either in the presence or absence of atropine) sinus node automaticity is less affected than AV conduction when verapamil is given parenterally. We propose that this greater negative dromotropic effect of verapamil is also in part due to a rate-dependent process, since during sinus rhythm AV junctional cells have to be depolarized at frequencies significantly higher than their intrinsic rates.

Atrioventricular nodal accommodation: rate- and time-dependent effects

1987 ◽  
Vol 252 (3) ◽  
pp. H578-H584 ◽  
Author(s):  
J. M. Loeb ◽  
J. M. deTarnowsky ◽  
C. C. Whitson ◽  
M. R. Warner
Keyword(s):  
Single Step ◽  
Time Dependent ◽  
Cumulative Effects ◽  
Similar Degree ◽  
Conduction Time ◽  
Atrial Pacing ◽  
Av Node ◽  
Absolute Level ◽  
Av Conduction ◽  
Multiple Step

To characterize intrinsic rate- and time-dependent properties of the atrioventricular (AV) node, we examined whether AV interval (AVI) would be comparable at identical heart rates (HR) reached using different types of stimulation paradigms. We compared changes in AVI during five consecutive 30-s, 20 beat/min increases in HR from control with AVI changes induced by 30-s single-step protocols to each of the same levels. In addition, HR was maintained at each level for 30, 60, 90, 120, and 150 s to control for the influences of time. Chloralose-anesthetized dogs (n = 16) were autonomically decentralized and instrumented to record electrocardiogram, blood pressure, and multiple intracardiac electrograms. Computer-generated HR steps were begun 20 beats/min above control, while continuously recording AVI. The beat-by-beat changes in AVI within each step were quantitated for all protocols. Differences between AVI during single- and multiple-step protocols were most pronounced during the first 15 s of atrial pacing. Accommodation in AVI (change in AV conduction time associated with an increased but constant heart rate) was evident during both protocols. The degree of accommodation during multiple-step protocols was modulated by the cumulative effects of earlier HR; however, a similar degree of accommodation occurred at higher HR irrespective of protocol used. Finally, the time to onset of loss of 1:1 AV conduction was significantly shorter when HR was increased using a multiple-step protocol. Thus the intrinsic response of the AV node to HR change is dependent on absolute level of HR, duration of rate change, and the potential cumulative effects of any earlier HR steps.

Effects of physiological aging on cardiac electrophysiology in perfused Fischer 344 rat hearts

1992 ◽  
Vol 262 (1) ◽  
pp. H97-H105 ◽  
Author(s):  
O. Schmidlin ◽  
S. Bharati ◽  
M. Lev ◽  
J. B. Schwartz
Keyword(s):  
Heart Rate ◽  
Age Differences ◽  
Cardiac Electrophysiology ◽  
Histopathological Examination ◽  
Conduction Time ◽  
Fischer 344 Rats ◽  
Aging Effects ◽  
Middle Aged ◽  
Fischer 344 ◽  
Av Conduction

Aging effects on heart rate and atrioventricular (AV) conduction were studied in Langendorff-perfused hearts from 18 mature (4-6 mo), 12 middle-aged (12-14 mo), and 18 senescent (24-26 mo) Fischer 344 rats. Heart rate decreased with increasing age from 218 +/- 18 in mature to 196 +/- 27 (mean +/- SD) beats/min in middle-aged rats to 183 +/- 22 beats/min in senescent rats (analysis of variance, P less than 0.001). Spontaneous AV conduction time increased from 43 +/- 7 to 49 +/- 5 to 62 +/- 9 ms with aging (P less than 0.0001). Paced AV conduction time also lengthened with aging, and AV Wenckebach block cycle length increased from 122 +/- 10 to 133 +/- 9 to 152 +/- 16 ms (P less than 0.005). Intra-atrial conduction time was unaffected by age. Age differences in heart rate and AV conduction responses to isoproterenol (0.5 x 10(-9) to 1 x 10(-7) M) were noted with greater sensitivity at lower doses in hearts from younger rats. In separate experiments, 18 mature and 19 senescent Fischer 344 rats received reserpine (0.25 mg.kg-1.day-1 ip) for 6 days before study. Age differences in heart rate and AV conduction persisted (P less than 0.0001). Histopathological examination of AV nodal and His-bundle tissues in three hearts from each age group showed increased intercellular collagen with advancing age.(ABSTRACT TRUNCATED AT 250 WORDS)

Critical prolongation of AV conduction time as the inciting mechanism in reentrant tachycardia

1972 ◽  
Vol 5 (1) ◽  
pp. 39-46 ◽  
Author(s):  
William J. Mandel ◽  
Alan I. Kermaier ◽  
Robert L. Blum ◽  
H. Hayakawa
Keyword(s):  
Conduction Time ◽  
Reentrant Tachycardia ◽  
Av Conduction

Coronary dilation with carotid chemoreceptor stimulation in cardiac-denervated dogs

1988 ◽  
Vol 255 (6) ◽  
pp. H1330-H1335
Author(s):  
Masayoshi Nagata ◽  
Robert Pichet ◽  
Michel Lavallee
Keyword(s):  
Adrenergic Receptors ◽  
Conscious Dogs ◽  
Base Line ◽  
Adrenergic Blockade ◽  
Coronary Resistance ◽  
Coronary Vasodilation ◽  
Similar Extent ◽  
Cardiac Denervation ◽  
Coronary Dilation ◽  
Cardiac Nerves

The coronary vasodilation that is secondary to carotid chemoreceptor stimulation (CCS) was compared in normal (N) and in cardiac-denervated (CD) conscious dogs. Under base-line conditions, CD only differed from N dogs by greater ( P ≤ 0.01) increases in mean arterial pressure (MAP) with CCS. Coronary blood flow (CBF) increased similarly in N (146 ± 18%) and CD (126 ± 15%) dogs, and coronary resistance (CR) fell to a similar extent in N (53 ± 3%) and CD (43 ± 5%) dogs. After muscarinic and β-adrenergic blockade, CCS resulted in similar increases in MAP in N and CD dogs; increases in CBF averaged 122 ± 15 and 115 ± 12% in N and CD dogs, respectively. Decreases in CR with CCS averaged 46 ± 3 and 40 ± 5% in N and CD dogs, respectively. α1-Adrenergic blockade prevented the increases in MAP with CCS and resulted in smaller (P < 0.01) increases in CBF, similar in N (77 ± 13%) and in CD (69 ± 10%) dogs. CR fell to the same extent in N (40 ± 4%) and CD (37 ± 5%) dogs. Additional blockade of agr2-adrenergic receptors further limited the increases in CBF with CCS in N (20 ± 5%) and CD (28 ± 7%) dogs; decreases in CR were attenuated similarly in N (13 ± 5%) and CD (21 ± 5%) dogs. Thus, in conscious dogs, cardiac nerves contribute little to the coronary dilation after carotid chemoreceptor stimulation. chemoreflex; α-adrenergic receptors; cardiac denervation Submitted on January 11, 1988 Accepted on July 28, 1988

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.

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