Intrinsic heart rate in the dog determined by pharmacologic denervation

1983 ◽  
Vol 245 (4) ◽  
pp. H592-H597 ◽  
Author(s):  
J. R. Brunsting ◽  
H. A. Schuil ◽  
W. G. Zijlstra
Keyword(s):  
Heart Rate ◽  
Blood Gases ◽  
Conscious Dogs ◽  
Interindividual Variation ◽  
Adrenergic Blockade ◽  
Intrinsic Heart Rate ◽  
Parasympathetic System ◽  
Autonomic Blockade ◽  
Cervical Vagotomy ◽  
The Difference

Intrinsic heart rate was measured in 19 dogs in 76 experiments after autonomic blockade, using various forms of anesthesia. Measurements were made in conscious dogs (n = 16) and in dogs in neuroleptanesthesia (n = 54) or under pentobarbital sodium (n = 6). Temperature, arterial pH, and blood gases were kept within narrow limits. Adrenergic blockade was achieved by phenoxybenzamine (2 mg X kg-1) and propranolol (2 mg X kg-1, followed by 2 mg X kg-1 X h-1). The parasympathetic system was blocked either by atropine (0.5 mg X kg-1, followed by 0.5 mg X kg-1 X h-1) and hexamethonium (20 mg X kg-1, followed by 10 mg X kg-1 X h-1) or by atropine and bilateral cervical vagotomy. Administration of hexamethonium or vagotomy was needed to block the vagal cardioacceleration unmasked by the administration of muscarinic blocking agents in conscious dogs and in dogs in neuroleptanesthesia. The mean denervated heart rate was 142.8 beats/min. This value is higher than that reported for surgically denervated hearts, the difference very likely reflecting the activity of the intact parasympathetic intrinsic cardiac innervation in surgical preparations. The estimated intraindividual and interindividual SD were 9.7 and 19.4 beats/min, respectively. The highly significant interindividual variation (P less than 0.01) contradicts the concept of an intrinsic heart rate as a practically constant species-dependent quantity.

alpha-Adrenergic control of oxygen delivery to myocardium during exercise in conscious dogs

1982 ◽  
Vol 242 (5) ◽  
pp. H805-H809 ◽  
Author(s):  
G. R. Heyndrickx ◽  
P. Muylaert ◽  
J. L. Pannier
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Oxygen Delivery ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Adrenergic Blockade ◽  
Adrenergic Control

alpha-Adrenergic control of the oxygen delivery to the myocardium during exercise was investigated in eight conscious dogs instrumented for chronic measurements of coronary blood flow, left ventricular (LV) pressure, aortic blood pressure, and heart rate and sampling of arterial and coronary sinus blood. After alpha-adrenergic receptor blockade a standard exercise load elicited a significantly greater increase in heart rate, rate of change of LV pressure (LV dP/dt), LV dP/dt/P, and coronary blood flow than was elicited in the unblocked state. In contrast to the response pattern during control exercise, there was no significant change in coronary sinus oxygen tension (PO2), myocardial arteriovenous oxygen difference, and myocardial oxygen delivery-to-oxygen consumption ratio. It is concluded that the normal relationship between myocardial oxygen supply and oxygen demand is modified during exercise after alpha-adrenergic blockade, whereby oxygen delivery is better matched to oxygen consumption. These results indicate that the increase in coronary blood flow and oxygen delivery to the myocardium during normal exercise is limited by alpha-adrenergic vasoconstriction.

Reflexes from isolated carotid sinuses of intact and vagotomized conscious dogs

1980 ◽  
Vol 238 (6) ◽  
pp. H815-H822 ◽  
Author(s):  
R. B. Stephenson ◽  
D. E. Donald
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Response Curve ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Stimulus Response ◽  
Carotid Baroreflex ◽  
Cervical Vagotomy ◽  
Curve Upward ◽  
Sinus Pressure

Exposure of the vascularly isolated carotid sinuses of 8 conscious dogs to static pressures between 50 and 240 mmHg caused significantly smaller increases [23 +/- 5(SE) mmHg] than decreases (37 +/- 4 mmHg) in arterial pressure frossure and heart rate and shifted the stimulus-response curve upward. Bilateral cervical vagotomy in conscious dogs caused sustained (3 h) increases in arterial pressure (40 +/- 5 mmHg), significantly larger than after atropinization (7 +/- 2 mmHg). In anesthetized, but not in conscious dogs, high sinus pressure reversed the hypertension caused by vagotomy. After vagotomy, low sinus pressure resulted in arterial pressures greater than 200 -mHg. In conscious dogs the carotid baroreflex can widely vary arterial pressure and heart rate despite buffering by extracarotid baroreceptors with vagal afferents, but cannot fully compensate for the acute loss of the latter. Extracarotid baroreceptors actively participate with carotid baroreceptors in the regulation of arterial pressure and better buffer carotid baroreflex-induced increases than decreases in arterial pressure.

Afferent vascular resistance control during hemorrhage in normal and autonomically blocked rabbits

1991 ◽  
Vol 261 (2) ◽  
pp. H380-H391 ◽  
Author(s):  
C. A. Courneya ◽  
P. I. Korner ◽  
J. R. Oliver ◽  
R. L. Woods
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Afferent Input ◽  
Ang Ii ◽  
Local Response ◽  
Simple Addition ◽  
Autonomic Blockade ◽  
The Difference ◽  
Constrictor Response

We examined the role of the arterial and cardiac baroreceptors on the hindquarter conductance and heart rate responses of conscious rabbits bled at approximately 3% blood volume (BV)/min to 80% BV (i.e., 20% BV removed). We used rabbits with both sets of baroreceptors working and when only one or neither sets was working. Each animal was studied with normal effector function and during autonomic blockade (hormonal + local effectors), where release of arginine vasopressin (AVP) and renin (angiotensin II, ANG II) were enhanced. The local response (LR) to hemorrhage was determined in a separate group of neurohumorally blocked rabbits. The estimated constrictor response (ECR) was the difference between the LR and net conductance response. In normal rabbits, the ECR was 49 units, with the estimated arterial-to-cardiac barorecptor drive ratio approximately 2.8:1 and with the two receptor groups acting by simple addition. Both barorecptors contributed to the rise in heart rate, with the relative arterial-to-cardiac baroreceptor drive ratio approximately 4:1. When hemorrhage was performed during autonomic blockade, ECR was 84 units (compared with normal rabbits, P less than 0.01), but blood pressure was poorly maintained and the constrictor effect was not under baroreceptor control. Although the baroreceptors were critical for AVP release during autonomic blockade, they played no role in renin release (ANG II production); the latter was released in large amounts, producing near-maximum constriction, which was unrelated to the afferent input. Thus neurally mediated regulation during hemorrhage has substantial advantages over that mediated primarily through the pressor hormones.

Baroreflex control of heart interval in conscious renal hypertensive dogs

1981 ◽  
Vol 241 (3) ◽  
pp. H332-H336
Author(s):  
M. D. Thames ◽  
C. L. Eastham ◽  
M. L. Marcus
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Hypertension ◽  
Conscious Dogs ◽  
Adrenergic Blockade ◽  
Cholinergic Mechanisms ◽  
Baroreflex Control ◽  
Control Heart ◽  
Before And After ◽  
Autonomic Blockade

The purpose of this study is to determine if baroreflex control of heart interval is abnormal in conscious dogs with renal hypertension. Changes in heart interval in response to transient nitroglycerin-induced decreases in arterial pressure and transient phenylephrine-induced increases in arterial pressure were determined in nine normotensive [mean arterial pressure 92 +/- 4 (SE) mmHg] and nine renal hypertensive conscious dogs (mean arterial pressure 139 +/- 10 mmHg). Data were acquired before and after beta-adrenergic blockade with 2 mg/kg iv propranolol and before and after parasympathetic blockade with 0.5 mg/kg iv atropine. Control heart rates for the normotensive and hypertensive dogs were not different (91 +/- 4 and 93 +/- 7 beats/min, respectively). Before autonomic blockade, the responses of normotensive and hypertensive dogs to nitroglycerin were not different. However, prolongation of the heart interval in response to phenylephrine in hypertensive dogs was significantly less than in normotensive dogs. In both groups, atropine nearly abolished the decrease in heart interval in response to nitroglycerin and the increase in heart interval in response to phenylephrine, although there were small but significant residual responses. Propranolol was without significant effect on heart interval responses to nitroglycerin and phenylephrine. We conclude that the baroreflex control of heart interval during transient decreases in arterial pressure is preserved in hypertensive dogs and is mediated mainly by decreases in parasympathetic outflow to the heart. In contrast, baroreflex control of heart interval during transient increases in arterial pressure is impaired in hypertension and is mediated mainly by activation of parasympathetic cholinergic mechanisms.

Sustained interruption of the aortic baroreflex by left cervical vagotomy in dogs

1984 ◽  
Vol 246 (3) ◽  
pp. H319-H323 ◽  
Author(s):  
S. C. Walgenbach
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Conscious Dogs ◽  
Conscious Dog ◽  
Bilateral Carotid ◽  
Cervical Vagotomy

Previous experiments demonstrated that acute left vagotomy interrupted 90% of the aortic baroreflex. The present study determined whether or not this interruption was sustained over a period of weeks. Bilateral carotid occlusions (BCO) were performed in conscious dogs before and for 3 wk after left vagotomy and immediately after subsequent right vagotomy. Prior to left vagotomy, BCO induced a rise in arterial pressure of 28 +/- 8 mmHg but no change in heart rate. After left vagotomy, BCO resulted in a rise in arterial pressure of 71 +/- 7 mmHg and a rise in heart rate of 43 +/- 6 beats/min. The BCO-induced elevations in arterial pressure and heart rate did not change significantly during the next 3 wk. Subsequent right vagotomy did not alter the rise in arterial pressure to BCO. These data indicate that left cervical vagotomy interrupts the aortic baroreflex for at least a 3-wk period and suggest that this procedure, when combined with reversible vascular isolation of the carotid sinuses, provides a method for studying cardiovascular adaptation to the acute loss of sinoaortic reflexes in the conscious dog.

P4423Extreme bradycardia in athletes is due to intrinsic changes within the heart

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M D Flannery ◽  
F Sully ◽  
K Janssens ◽  
G Morris ◽  
J Kalman ◽  
...  
Keyword(s):  
Heart Rate ◽  
Vagal Tone ◽  
Endurance Athletes ◽  
Valsalva Manoeuvre ◽  
Resting Heart Rate ◽  
Maximum Heart Rate ◽  
Vo2 Max ◽  
Heart Rates ◽  
Intrinsic Heart Rate ◽  
Autonomic Blockade

Abstract Background It is well known that athletes and in particular endurance athletes have lower resting heart rates than non-athletes. This has generally been considered a healthy adaptation. Traditionally this was thought be due to increased vagal tone. Several studies have shown that endurance athletes continue to have lower heart rates in the absence of autonomic influence suggesting bradycardia is due to intrinsic changes within the heart. A subset of endurance athletes have very low heart rates with Tour de France cyclists having described heart rates in the 30s. It is unclear whether in these elite athletes with very low heart rates the profound bradycardia is due to autonomic influence or intrinsic changes within the heart. Aim The aim of this study was to determine if extreme bradycardia in athletes is due to excess vagal tone or more profound intrinsic changes within the heart. Methods We recruited three cohorts for this study: non-athlete controls (NA), endurance athletes with a documented resting heart rate >40 (EA) and endurance athletes with a resting heart rate <40 (BA). All participants underwent baseline testing including ECG, echocardiography and VO2 max testing. All participants came back on a second occasion for treatment with dual autonomic blockade (DAB) to determine intrinsic heart rate in the following manner. After resting supine for five minutes resting heart rate was measured. Participants were then administered 0.04mg/kg of intravenous atropine. After five minutes participants were then administered 0.05mg/kg of intravenous metoprolol. This was repeated every five minutes until there was no further drop in heart rate or 0.2mg/kg had been administered. The resting heart rate at this stage was recorded as the intrinsic heart rate. Parasympathetic blockade was confirmed by lack of response to Valsalva manoeuvre and sympathetic blockade was confirmed by lack of response to metoprolol. VO2 max testing was then performed to determine maximum heart rate. Results 9 NA (7 male), 10 EA (8 male) and 5 BA (4 male) participated in this study. The average age was similar in all groups (NA 32.9y, EA 32.4y, BA 31.4y). The average resting heart rate was 71.7 in the NA group, 48.3 in the EA group and 41.6 in the BA group (p<0.05 for comparisons between all three groups). Following dual autonomic blockade resting heart rate was 86.0 in the NA group, 76.9 in the EA group and 64.4 in the BA group (p<0.05 for comparisons between all three groups). Maximum heart rate under DAB was 140.1 in the NA group, 138.0 in the EA group and 140.4 in the BA group. These differences were not significant. Conclusion In athletes with very low heart rates, bradycardia is due to more profound intrinsic changes within the heart. Acknowledgement/Funding NHMRC Project Grant

Effect of vasopressin and phenylephrine on arterial pressure and heart rate in conscious dogs

1986 ◽  
Vol 251 (2) ◽  
pp. H253-H260
Author(s):  
J. L. Robinson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Response Curve ◽  
Baroreflex Sensitivity ◽  
Conscious Dogs ◽  
Baroreflex Control ◽  
Pressure Stimulus ◽  
Before And After ◽  
Autonomic Receptors ◽  
The Difference

The effect of arginine vasopressin (AVP) and phenylephrine (PE) infusions on mean arterial pressure (MAP) and heart rate (HR) were compared in conscious dogs with all autonomic receptors intact (I), during muscarinic blockade (MB) and during ganglionic blockade (GB). After either MB or GB, the dose-MAP response curve for AVP and PE was shifted to the left of the I response curve; a greater shift was observed with AVP than with PE. The MAP threshold after GB for AVP and PE occurred at 10 and 50% of the threshold dose observed during the I response, respectively. Not only did the MAP threshold occur at a lower dose after MB and GB, but also the slope of the response curve was steeper than that of the I response. Comparing the amount of drug necessary to increase MAP 25 mmHg above control for PE and AVP before and after GB, the intact PE response required 4.3 +/- 1.0 (P less than 0.01) times more drug than during GB versus the intact AVP required 16.8 +/- 2.8 (P less than 0.01) times more drug than during GB. The baroreflex control of HR when all receptors were intact was 3.4 +/- 0.4 (P = 0.001) times more sensitive during AVP compared with PE; no differences were observed after MB. There were no significant changes in HR to AVP or PE after GB, thus indicating a lack of a direct effect of these agents on the HR. Our results show that MB and GB equally potentiate the pressor effects of AVP and PE, and the augmentation was much greater for AVP than for PE. The difference in the potentiation of these two vasoconstrictors is consistent with the finding that the baroreflex sensitivity during AVP was enhanced compared with PE. We have postulated that, in the resting conscious dog, AVP increases the sensitivity of the baroreflex primarily by producing a greater level of parasympathetic tone to the heart in response to a given pressure stimulus.

Uneven blunting of chronotropic baroreflexes in obese Zucker rats

1989 ◽  
Vol 256 (2) ◽  
pp. H417-H421 ◽  
Author(s):  
D. L. Barringer ◽  
R. D. Bunag
Keyword(s):  
Heart Rate ◽  
Female Rats ◽  
Zucker Rats ◽  
Adrenergic Blockade ◽  
Sprague Dawley ◽  
Heart Rates ◽  
Reflex Tachycardia ◽  
Mean Pressure ◽  
Autonomic Blockade ◽  
Obese Zucker Rats

We compared reflex chronotropic responses to intravenously infused drugs in three groups of age-matched normotensive female rats, namely, Sprague-Dawley, lean Zucker, and obese Zucker. Initial mean pressures did not differ between rat groups, but heart rates tended to be lower in obese Zucker rats. Baroreflex impairment was already evident, because heart rate responses to infused phenylephrine (reflex bradycardia) or sodium nitroprusside (reflex tachycardia) were consistently weaker in obese Zucker than in other rats. Regardless of rat grouping, subsequent cholinergic blockade with atropine elevated, whereas beta-adrenergic blockade with propranolol lowered, basal heart rates without affecting mean pressure. Reflex heart rate responses were all appreciably reduced after either type of autonomic blockade, and although the extent of inhibition varied between rat groups, the residual heart rate responses remaining after blockade were nonetheless always smaller in obese than in lean rats. This difference suggests that efferent sympathetic and parasympathetic mechanisms normally responsible for mediating heart rate reflexes were unevenly blunted in obese Zucker rats.

Autoresuscitation: a survival mechanism in piglets

1992 ◽  
Vol 73 (2) ◽  
pp. 749-753 ◽  
Author(s):  
U. M. Sanocka ◽  
D. F. Donnelly ◽  
G. G. Haddad
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Tidal Volume ◽  
Blood Gases ◽  
Mean Blood Pressure ◽  
Inspiratory Time ◽  
Stimulus Period ◽  
Autonomic Blockade ◽  
Electroencephalogram Eeg ◽  
Arterial Po2

Piglets were studied to determine 1) the cardiovascular and neurophysiological effects of prolonged laryngeal-induced respiratory inhibition (n = 7) and 2) whether these effects were modulated by autonomic blockade (n = 6). Respiration, electrocardiogram, electroencephalogram (EEG), and blood pressure were recorded, and blood gases were measured. During continuous laryngeal stimulation in the presence of light anesthesia, apnea was interrupted every 1–2.5 min by clusters of two to six breaths. Compared with control, these breaths had a significantly greater tidal volume (430 +/- 30% of control), shorter inspiratory time (87 +/- 5%), and longer expiratory time (124 +/- 15%) and, thus, were of a gasping nature. With each cluster of gasps, arterial PO2 increased from 15 +/- 2 to 56 +/- 5 Torr, heart rate from 84 +/- 7 to 161 +/- 5 beats/min, and mean blood pressure from 48 +/- 4 to 106 +/- 6 mmHg. The EEG became flat by 1 min after the onset of apnea and remained isoelectric throughout the stimulus period. Cyclical gasps were not affected by sympathetic or parasympathetic blockade. These data show that, despite EEG silence, piglets can autoresuscitate by initiating gasps that are not dependent on autonomic integrity. These gasps markedly improve cardiovascular status and may sustain animals for a prolonged period of time.

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