Alternative mechanism of cardiac acceleration in Bainbridge's infusion experiments

Pathak, C. L.

doi:10.1152/ajplegacy.1959.197.2.441

Cited by 23 publications

(12 citation statements)

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“…The manner in which the pacemaker cells are influenced by stretch to change their frequency is not clear, though some investigators claim that the pacemaker frequency may be primarily dependent on the tension in the pacemaker cells (PATHAK, 1959;JAMES and NADEAU, 1963).…”

Section: Discussionmentioning

confidence: 99%

“…It has long been known that distension of mammalian atrial tissues including the sinoatrial (SA) node produces an acceleration of heart rate (BAINBRIDGE,1915;SASSA and MIYAZAKI, 1920;SCHERF et al, 1949;HOLLANDER and WEBS, 1955;BLINKS, 1956;PATHAK, 1959) which appears to be due to a direct action on the pacemaker cells. Brooks and his coworkers LANGE et al, 1966) studied the effect of stretch on the discharge rate of in situ or isolated mammalian SA nodal region and suggested that the stretch-induced acceleration of pacemaker activity is mediated by a lowering of membrane potential caused by an increase in Na permeability, while extrinsic nerves are not essential to this reaction.…”

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confidence: 99%

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Length-dependent changes of pacemaker frequency in the isolated rabbit sinoatrial node.

1984

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To correlate changes in pacemaker frequency with those of length and tension in mammalian atrial tissues, a strip of the sinoatrial (SA) nodal tissue (about 10 mm in length and 4 mm in width) isolated from the rabbit heart was subjected to constant-length and constantload stretches, and the relation between the resulting pacemaker frequency changes and the segmental length changes of the preparation was examined by means of cinematographic recording of the preparation with carbon markers on its surface. The amount of stretch-induced length changes was larger in the perinodal tissue segments than in the SA nodal segments, indicating that the nodal area is less extensible than the perinodal area. The time course of stretch-induced length changes of one nodal segment (closer to the inferior versa cava) was found to roughly parallel that of pacemaker frequency changes, suggesting that the pacemaker frequency is primarily dependent on the length but not on the tension of the SA nodal area.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Length-dependent changes of pacemaker frequency in the isolated rabbit sinoatrial node.

1984

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“…For example, we found that heart rate still increased with volume loading after simple beta-receptor blockade but not after combined beta-receptor and cholinergic blockade or after cholinergic blockade alone. Although it has been suggested that volume loading induces a direct positive chronotropic effect (18)(19)(20), the data obtained in the present study in the dogs studied several days after recovery from bilateral vagotomy indicate that this mechanism, if present, must be minor, since heart rate failed to rise with volume loading in these dogs even though control rates were only 114 ± 3 beats/min, a level considerably less than that observed with either moderate volume loading (148 ± 1 1 beats/min) or maximum volume loading (178 ± 5 beats/min) in the intact conscious dogs.…”

Section: Discussionmentioning

confidence: 99%

Reduced baroreflex sensitivity with volume loading in conscious dogs.

Vatner

D²,

Heyndrickx³

et al. 1975

Circulation Research

108

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The Bainbridge reflex, i.e., the effect of rapid saline infusion (1.1 ± 0.1 liters) on heart rate and arterial and atrial blood pressures, was examined in 12 intact conscious dogs; mean arterial blood pressure rose by 33 ± 3 (SE) mm Hg, mean atrial pressure by 14 ± 1 mm Hg, and heart rate by 75 ± 9 beats/min. After beta-receptor blockade, heart rate rose slightly less (+49 =t 5 beats/min, P = 0.05). Cholinergic blockade, combined cholinergic and beta-receptor, or beta-receptor blockade after vagotomy blocked the heart rate response to the infusion. The rise in heart rate in the face of an increase in arterial blood pressure with volume loading suggested that the arterial baroreceptor reflex was not responding appropriately to the increase in arterial blood pressure. In conscious dogs after denervation of the arterial baroreceptors, the increase in heart rate with volume loading was no greater than that in those dogs with their arterial baroreceptors intact, suggesting that the baroreceptor reflex was not restraining heart rate in the normal response to volume loading. The relationship between the pulse interval (PI) and the systolic arterial blood pressure (SAP) following an intravenous injection of methoxamine was used to evaluate the sensitivity of the baroreceptor reflex in intact conscious dogs. After a mild amount of volume loading, when atrial pressure was 8 ± 2 mm Hg, the PI/SAP slope was significantly depressed from normal. When atrial pressure was elevated further to 28 ± 1 mm Hg by volume loading, the slope was further depressed. Thus, arterial baroreflex sensitivity is reduced progressively as atrial pressure is raised by volume loading, an observation that explains how heart rate can rise strikingly in the face of an elevated arterial blood pressure.• In 1915, Bainbridge (1) observed that a rapid infusion of saline or blood induces tachycardia, which is abolished by vagotomy; this response has been referred to as the Bainbridge reflex. The Bainbridge reflex is one of several physiological situations that does not follow Marey's law (2), which describes the inverse relationship between cardiac rate and arterial blood pressure, since volume loading results in an increase in both arterial blood pressure and cardiac rate. The infusion-induced elevation of arterial blood pressure would be expected to stimulate the arterial baroreceptors to reduce heart rate reflexly, unless a change in the gain of the reflex, the set point of the reflex, or both occurs (3). The goal of the present study was to evaluate the effects of acute volume 236loading on heart rate in the conscious dog and to examine the extent to which volume loading alters the properties of the arterial baroreceptor system.Since one of the controversies concerning the Bainbridge reflex involves the questions of whether heart rate consistently rises with volume loading and to what extent the response is related to the initial heart rate prior to volume loading (4-6), the present study was conducted in conscious dogs in which resting heart ...

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“…The observation of postvagal tachycardia in the isolated heart preparation of the rabbit excludes the possibility that this cardioacceleration is due, in the intact animal, to the mechanical stretch of sinu-atrial node pace-maker cells by an increase in right atrial pressure during and after vagal stimulation (McDowall, 1956;Pathak, 1959).…”

Section: Discussionmentioning

confidence: 99%

An experimental analysis of the tachycardia that follows vagal stimulation

Burke¹,

Calaresu²

1972

The Journal of Physiology

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SUMMARY1. Postvagal tachycardia, the transient increase in heart rate that follows the sinus bradycardia elicited by vagal stimulation, was investigated in thirty chloralosed cats. Maximum postvagal tachycardia was elicited by stimulation at frequencies of Hz with train durations of 30-90 sec. A positive correlation was demonstrated between the magnitudes of postvagal tachycardia and of the preceding sinus bradycardia.2. Postvagal tachycardia was not affected by either spinal transaction at C7 or by administration of propranolol (1-5 mg/kg i.v.), but was abolished by the administration of atropine (2.0 mg/kg i.v.).3. Postvagal tachycardia was observed to follow the vagal bradycardia induced reflexly either by administration of phenyldiguanide (100-300 jug i.v.) or by stimulation of the aortic depressor nerve.4. In the isolated atria-vagus preparations from six rabbits a positive correlation was demonstrated between the magnitude of postvagal tachycardia and of the preceding bradyeardia elicited by vagal stimulation.5. Continuous intracellular recordings were obtained from four sinuatrial node pace-maker cells in the isolated atria-vagus preparation of the rabbit before, during and after vagal stimulation. During postvagal tachycardia the slope of the diastolic prepotential, the maximum diastolic potential, threshold potential and the overshoot were found to be increased; these changes are different from those found in pace-maker cells during adrenergic activation.6. These findings demonstrate that postvagal tachycardia is not mediated by sympathetic adrenergic mechanisms, but suggest that it is dependent upon the preceding vagal bradycardia and may be related to an increase in net sodium influx into pace-maker cells initiated by the hyperpolarization of the pace-maker cell membrane during and immediately after vagal stimulation.

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Alternative mechanism of cardiac acceleration in Bainbridge's infusion experiments

Cited by 23 publications

References 0 publications

Length-dependent changes of pacemaker frequency in the isolated rabbit sinoatrial node.

Length-dependent changes of pacemaker frequency in the isolated rabbit sinoatrial node.

Reduced baroreflex sensitivity with volume loading in conscious dogs.

An experimental analysis of the tachycardia that follows vagal stimulation

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