"Summation" of the increase in heart rate from stimulation of atrial receptors

1980 ◽  
Vol 58 (6) ◽  
pp. 666-672
Author(s):  
P. V. Greenwood ◽  
C. T. Kappagoda
Keyword(s):  
Heart Rate ◽  
Left Atrial ◽  
Superior Vena ◽  
Right Atrial ◽  
Propranolol Hydrochloride ◽  
Superior Vena Caval ◽  
The Right ◽  
Atrial Receptors ◽  
Stimulation Of ◽  
Wire Cage

In dogs anaesthetized with chloralose, application of stimuli which are likely to activate left atrial (L.A.) and right atrial (R.A.) receptors (complex unencapsulated endings) has been shown to result in an increase in heart rate. The present investigation was undertaken to determine whether the response elicited by the application of one stimulus (i.e., to the left atrium) could be enhanced by the application of a second stimulus (i.e., to the right atrium) in the same animal.The L.A. receptors were stimulated by distending a small balloon at the right upper pulmonary vein-L.A. junction and the R.A. receptors by "expanding" a spherical wire cage positioned at the superior vena caval (S.V.C.)-R.A. junction. Pressures in the S.V.C., R.A., L.A., and femoral artery were measured and the electrocardiogram monitored.In eight dogs stimulation of L.A. receptors resulted in an increase in heart rate (H.R.) of 18.5 beats/min (SEM 6.0; N = 23). In the same animals stimulation of R.A. receptors resulted in an increase in H.R. of 14.6 beats/min (SEM 2.0; N = 25). Application of both stimuli simultaneously resulted in an increase of 32.2 beats/min (SEM 8.0; N = 13). In four dogs propranolol hydrochloride (0.5 mg/kg) markedly diminished the response. In three dogs the response was abolished by bretylium tosylate (10 mg/kg).It is concluded that the increase in H.R. resulting from the application of these two stimuli could be "summated" and these findings support the proposition that the receptors in the two atria act as a functional entity.

Effect of cervical vagal stimulation on chicken heart rate and atrioventricular conduction

1983 ◽  
Vol 244 (2) ◽  
pp. R235-R243
Author(s):  
J. M. Goldberg ◽  
M. H. Johnson ◽  
K. D. Whitelaw
Keyword(s):  
Heart Rate ◽  
Vagal Stimulation ◽  
Atrioventricular Conduction ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Chicken Heart ◽  
Av Conduction ◽  
Supramaximal Stimulation ◽  
The Right ◽  
Stimulation Of

The effects of supramaximal stimulation of the right and left cervical vagi on heart rate, pacemaker localization, and atrioventricular (AV) conduction were investigated in 15 anesthetized open-chest chickens before and after atropine sulfate. Epicardial bipolar electrograms were recorded from selected atrial sites and right ventricle. A back lead electrocardiogram was also recorded. The effect of stimulation on atrioventricular conduction was evaluated during pacing from one of the right atrial recording sites. Supramaximal stimulation of either cervical vagus produced bradycardia but not cardiac arrest. Heart rate was reduced from an average spontaneous rate of 282 +/- 13 (SE)/min to 161 +/- 13/min with stimulation of the right and left cervical vagus. Pacemaker shifts occurred in over 50% of the vagal stimulations. The most frequent shift occurred to the lower AV node or ventricles. Pacemaker shifts to the AV junctional region producing almost simultaneous activation of the atria and ventricles were not observed. Vagal stimulation during atrial pacing produced minimal prolongation in AV conduction time [right vagus, 13 +/- 3 (SE) ms; left vagus, 8 +/- 2 ms]. Second and third degree heart blocks were not observed during pacing. Vagal stimulation after atropine indicates that the cervical vagi do not contain sympathetic fibers going to pacemaker or AV conduction tissues.

Cardiac responses to electrical stimulation of discrete loci in canine atrial and ventricular ganglionated plexi

1990 ◽  
Vol 259 (5) ◽  
pp. H1365-H1373 ◽  
Author(s):  
C. K. Butler ◽  
F. M. Smith ◽  
R. Cardinal ◽  
D. A. Murphy ◽  
D. A. Hopkins ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Right Ventricular ◽  
Left Atrial ◽  
Right Atrial ◽  
Intramyocardial Pressure ◽  
Cardiac Responses ◽  
Ganglionated Plexi ◽  
The Right ◽  
Ganglionated Plexus ◽  
Stimulation Of

The purpose of the present study was to examine cardiac effects induced by electrical stimulation (1-4 V, 1 ms, 200 Hz) of discrete loci within the ganglionated plexi located on canine atria and ventricles. When 20 loci in the right atrial ventral ganglionated plexi of 11 anesthetized open-chest dogs were stimulated, bradycardia and/or right and left atrial force suppression occurred when, on average, 15% of these loci were stimulated. Bradycardia and atrial force suppression were elicited when, on average, 8% of 15 loci in the left atrial ventral ganglionated plexi of eight dogs was stimulated. When these loci were restimulated after acute decentralization, cardiac responses were attenuated or occasionally eliminated. After atropine (1 mg/kg iv) administration, repeat stimulation of loci in the right but not left atrial ganglionated plexus induced tachycardia. Stimulation of loci in the right ventricular ganglionated plexus after the subsequent administration of desipramine (1 mg/kg iv) in six dogs resulted in an increase in right ventricular conus intramyocardial pressure. After hexamethonium administration (10 mg/kg iv, followed by a continuous infusion of 1 mg.kg-1.min-1), sympathetic responses were no longer elicited from one of the five dogs in which loci in the right atrial ganglionated plexi and from two of the six dogs in which loci of the right ventricular ganglionated plexus had elicited responses. We conclude that atrial and ventricular ganglionated plexi contain efferent parasympathetic, efferent sympathetic, and afferent neurons.

Influence of venous injection sites on evolution of dilution curves in dogs

1963 ◽  
Vol 205 (3) ◽  
pp. 504-510
Author(s):  
Ramon L. Lange ◽  
James T. Botticelli
Keyword(s):  
Pulmonary Artery ◽  
Femoral Artery ◽  
Inferior Vena ◽  
Superior Vena ◽  
Right Atrial ◽  
Superior Vena Caval ◽  
Right Heart ◽  
Inferior Vena Caval ◽  
The Right ◽  
Dilution Curves

The role of venous passage of indicator from different venous injection sites on the genesis of right heart and pulmonary artery dilution curves was examined. Right heart and pulmonary artery thermodilution curves were recorded after injection of cool dye into commonly used portals—superior vena caval, right atrial, and inferior vena caval—and the contour compared with the subsequent femoral artery dye dilution curve. With superior vena caval or right atrial injection, the contour and disappearance slopes of the pulmonary artery curve bore an extremely variable relationship to those of the femoral artery curve. In sharp contrast, inferior vena caval injection yielded pulmonary artery curves with disappearance slopes which were highly correlated with the femoral artery slope ( r = .99). With inferior vena caval injection, considerable temporal dispersion and spatial dispersion of indicator is found at the right atrial level. With superior vena caval injection distribution mainly occurred beyond the right atrium and even beyond the pulmonary artery in eight out of ten animal studies. The geometry of the venous system may explain this difference. Inaccuracies in flow calculation from right heart dilution curves in dogs would seem to be minimized by inferior vena caval injection.

Effect of stretching the superior vena cava on heart rate in rats

1981 ◽  
Vol 241 (2) ◽  
pp. H248-H254 ◽  
Author(s):  
S. Kaufman ◽  
B. Mackay ◽  
C. T. Kappagoda
Keyword(s):  
Heart Rate ◽  
Histological Examination ◽  
Superior Vena Cava ◽  
Right Atrium ◽  
Superior Vena ◽  
Vena Cava ◽  
Nerve Endings ◽  
Sympathetic Blockade ◽  
Propranolol Hydrochloride ◽  
The Right

The effect on the heart rate of stretching the superior vena cava 3-4 mm above its entrance to the right atrium was examined in rats anesthetized with chloralose. The superior vena cava was stretched 41 times in 16 rats. There was a mean increase of 24.1 +/- 1.9 (SE) beats/min. This response was abolished (6 rats) by sympathetic blockade (with propranolol hydrochloride and bretylium tosylate) and by bilateral vagosympathectomy (5 rats). Application of lidocaine to the cervical vagi also abolished the response in a reversible manner (4 rats). In five rats, histological examination of the superior vena cava revealed an abundance of nerves, which formed a net in the stretched region. Complex unencapsulated nerve endings similar to those demonstrated in the dog and cat were not found.

Distribution of fetal cardiac output: importance of pacemaker location

1976 ◽  
Vol 231 (1) ◽  
pp. 204-208 ◽  
Author(s):  
PT Pitlick ◽  
SE Kirkpatrick ◽  
WF Friedman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Left Atrial ◽  
Left Ventricular ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Foramen Ovale ◽  
Rate Versus ◽  
Left Ventricular Output ◽  
The Right

Important questions exist about the relative roles of changes in heart rate versus extent of myocardial shortening in regulating fetal cardiac output, because increases in heart rate created by left atrial pacing have been shown to increase right ventricular output and decrease left ventricular output. Since the pacemaker site could importantly influence foramen ovale flow and, hence, each ventricle's output, changes in individual ventricular outputs were examined when both the right and left atria were paced at a rate of 270 beats/min in five acute and in eight chronically instrumented fetal lamb studies. With pacing of either atrium, total cardiac output was unchanged compared to control values. However, the right ventricle contributed more to total cardiac output with left atrial pacing (73% acute, 65% chronic) than with right atrial pacing (51% acute, 57% chronic). Converse changes were observed in left atrial pacing (27% acute, 35% chronic) as compared to right atrial pacing (49% acute, 43% chronic). Thus the disparity that exists normally in the contributions of the right and left ventricles to total cardiac output is accentuated with left atrial pacing and minimized with right atrial pacing. Pressure measurements demonstrated changes in the atrial pressure relations that would be expected to alter flow across the foramen ovale depending on the chamber initially activated. Previous experimental differences can, therefore, be attributed to changes in the magnitude of shunting across the foramen ovale and depend on pacemaker location.

Right atrial stretch decreases supraoptic neurosecretory activity and plasma vasopressin

1981 ◽  
Vol 241 (1) ◽  
pp. R44-R49
Author(s):  
R. P. Menninger
Keyword(s):  
Left Atrial ◽  
Supraoptic Nucleus ◽  
Right Atrial ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Neurosecretory Neurons ◽  
Plasma Arginine ◽  
Right Atrial Appendage ◽  
The Right ◽  
Atrial Receptors

It is generally held that left atrial stretch (LAS) but not right atrial stretch (RAS) reflexly inhibits vasopressin release and results in a diuresis. To reexamine the influence of RAS on the release of vasopressin and on the behavior of antidromically identified supraoptic neurosecretory neurons, RAS and LAS were applied in pentobarbital-anesthetized cats. Weighted 20 or 30 g sutures were placed in the left atrium pulmonary vein junction and at the base of the right atrial appendage. Antidromically identified supraoptic nucleus neurons were inhibited by both RAS and LAS applied independently and together, although fewer neurons were responsive to RAS alone. Simultaneous stretch of both atria resulted in greater inhibition of these neurons than did stretch of either atrium alone. Stretch of the right atrium alone also resulted in a significant decrease in plasma arginine vasopressin measured by radioimmunoassay. Differences between these results and other reports may stem from differences in the method of RAS or the specific right atrial receptors affected.

Cardiovascular afferent signals and drinking in response to hypotension in dogs

1999 ◽  
Vol 277 (3) ◽  
pp. R795-R801 ◽  
Author(s):  
Terry N. Thrasher ◽  
Craig R. Keenan ◽  
David J. Ramsay
Keyword(s):  
Pulmonary Artery ◽  
Water Intake ◽  
Left Atrial ◽  
Inferior Vena ◽  
Vena Cava ◽  
Ascending Aorta ◽  
Right Atrial ◽  
Arterial Hypotension ◽  
Atrial Receptors ◽  
Stimulation Of

Arterial hypotension stimulates increases in plasma arginine vasopressin (AVP), plasma renin activity (PRA), and water intake in conscious dogs. We have previously reported that increasing left atrial but not right atrial pressure completely blocks the increase in plasma AVP and PRA induced by hypotension. The goal of the present study was to examine the effect of increasing right or left atrial pressure on water intake induced by arterial hypotension. Dogs were prepared with occluding cuffs on the thoracic inferior vena cava, the pulmonary artery, and the ascending aorta. We reduced mean arterial pressure (MAP) 25% below control by either inferior vena cava constriction (IVCC), pulmonary artery constriction (PAC), or ascending aorta constriction (AAC) and measured water intake over a 2-h period. Cumulative water intake during IVCC ( n = 6) and PAC ( n = 6) was 7.8 ± 2.0 and 6.7 ± 2.6 ml/kg, respectively. There was no difference between either the latency or the volume consumed between the two treatments. In contrast, none of the dogs drank during hypotension induced by AAC ( n = 5). Because the degree of arterial baroreceptor unloading was the same in each treatment by design, we conclude that stimulation of left atrial receptors inhibits drinking in response to arterial hypotension but that stimulation of right atrial receptors has no effect on the response in dogs.

Effect of stimulating right atrial receptors on renal blood flow

1982 ◽  
Vol 60 (12) ◽  
pp. 1672-1679 ◽  
Author(s):  
F. Karim ◽  
S. Kaufman ◽  
C. T. Kappagoda
Keyword(s):  
Blood Flow ◽  
Renal Mass ◽  
Carotid Sinus ◽  
Superior Vena ◽  
Renal Perfusion ◽  
Right Atrial ◽  
Myelinated Fibres ◽  
Right Atrial Appendage ◽  
The Right ◽  
Atrial Receptors

This investigation was undertaken to determine the effect of stretching the superior vena caval – right atrial (SVC–RA) junction and the right atrial appendage on blood flow to the kidney (RBF) and to establish whether any changes observed were influenced by the input from the baroreceptors in the carotid sinus. The experiments were performed on seven dogs, anaesthetized with α-chloralose. The systemic arterial (i.e., renal perfusion) pressure was held constant. At a carotid sinus pressure (CSP) of 59.0 ± 1.2 mmHg (1 mmHg = 133.322 Pa), the RBF increased from 218 ± 16.1 to 231.7 ± 18.4 mL/min per 100 g renal mass (p < 0.025). At a CSP of 88.0 ± 3.5 mmHg, the RBF increased from 230.1 ± 19.2 to 237.1 ± 19.2 mL/min per 100 g renal mass (p < 0.05). At a CSP of 137 ± 3.7 mmHg there were no significant changes in RBF. These responses were abolished by cutting (four dogs) or cooling the vagi (one dog only). In a subsidiary investigation it was shown that stretching the SVC–RA junction activated receptors in the endocardial surface of the right atrium which discharged into myelinated fibres in the vagi, having an average conduction velocity of 8.1 m/s (range 3.8–15). It is concluded that stimulation of right atrial receptors increases the RBF and that this response is influenced by the input from the barorceptors in the carotid sinus.

Interaction of left atrial receptors and carotid sinus baroreceptors on heart rate in the dog

1985 ◽  
Vol 248 (5) ◽  
pp. H631-H636 ◽  
Author(s):  
K. K. Teo ◽  
G. C. Man ◽  
C. T. Kappagoda
Keyword(s):  
Heart Rate ◽  
Left Atrial ◽  
Carotid Sinus ◽  
Aortic Pressure ◽  
Response Curves ◽  
Stimulus Response ◽  
Alpha Chloralose ◽  
Atrial Receptors ◽  
Control State ◽  
Stimulation Of

This study was undertaken to determine the influence of 1) the left atrial receptors (LA) on the ability of the carotid sinus baroreceptors (CS) to regulate heart rate and 2) the CS on the reflex increase in heart rate mediated by the LA. The LA were stimulated by stretching the pulmonary vein-atrial junctions in dogs anesthetized with alpha-chloralose. Aortic pressure was controlled, and the pressure in the CS was regulated. Stimulus-response curves were obtained relating heart rate to pressures in the CS, in the control state, and during stimulation of LA (6 dogs). Factorial analysis revealed that LA exerted a significant influence on heart rate (P less than 0.01). Next the CS pressure was set at mid, low, and high levels and the LA stimulated. It was found that the effect on heart rate was greatest at the mid setting (+19.3 +/- 2.9 beats/min) and least at the low setting of the pressure in the CS (+0.9 +/- 0.5, 11 dogs). Sympathetic blockade attenuated significantly the response in the mid setting of the CS pressure and left intact the response at the high setting of the pressure in the CS. It is concluded that there is a significant interaction between these two reflexes.

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