The Mechanism of Adaptation of Left Atrial Stretch Receptors in Dogs with Chronic Congestive Heart Failure

Zucker, Irving H.; Earle, A. M.; Gilmore, J. P.

doi:10.1172/jci108780

Cited by 163 publications

(44 citation statements)

References 48 publications

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“…Another possibility is that the mechanoreceptors in patients with CHF are abnormal. Zucker et al 20 reported that atrial receptors were abnormal in the dog with induced heart failure. Carotid and aortic baroreceptor function could also be impaired in heart failure.21…”

Section: Discussionmentioning

confidence: 99%

The neurohumoral and hemodynamic response to orthostatic tilt in patients with congestive heart failure.

et al. 1983

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SUMMARY Thirty-five patients with varying degrees of congestive heart failure were subjected to 600 upright tilt. Eight of the patients with normal resting hemodynamics had elevated resting plasma norepinephrine levels (PNE) (p < 0.001), but their response to upright tilt was similar to that in normal subjects: All had increases in heart rate, plasma norepinephrine (from 263 ± 32 to 483 ± 78 pg/mg, p < 0.02) and plasma renin activity (from 4.8 ± 0.9 to 13.7 ± 7.6 ng/mI/hour, p < 0.05). In 27 patients with high resting pulmonary wedge pressure and low cardiac index, resting PNE was higher (668 ± 71 ng/ml), but PNE, plasma renin activity and heart rate did not increase significantly during tilt despite a fall in pulmonary capillary wedge pressure and cardiac index. In 18 of these patients, PNE rose during tilt, whereas in nine it did not change or fell; the regting hemodynamics and the hemodynamic response to tilt were not significantly different in these two groups. These data suggest that an abnormality of mechanoreceptor or baroreceptor function is common in patients with CHF. This abnormality corresponds in part to the severity of the resting hemodynamic abnormality, but among patients with severe CHF, the reflex neurohumoral abnormality may provide independent information about the severity of the disease.UPRIGHT TILT normally induces a fall in cardiac filling and stroke volume that elicits a neurohumoral response characterized by increases in circulating norepinephrine (PNE) levels and plasma renin activity (PRA).1' This neurohumoral response is thought to play an important role in the increases in heart rate and systemic vascular resistance that maintain arterial pressure in the upright position. The stimulus for this neurohumoral response appears to reside primarily in the cardiopulmonary area through mechanoreceptors at the junctions of the vena cava and right atrium and the pulmonary veins and left atrium, and in the left ventricle. The importance of this neurohumoral response in the support of arterial pressure is reflected by evidence that pharmacologic or pathologic inhibition of this response leads to orthostatic hypotension.7-lIn congestive heart failure (CHF), PNE is usually

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Section: Discussionmentioning

confidence: 99%

The neurohumoral and hemodynamic response to orthostatic tilt in patients with congestive heart failure.

et al. 1983

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“…We measured SNA, MAP, cardiac filling pressure (as either pulmonary artery pressure [PAP] or pulmonary capillary wedge pressure), and cardiac output responses during ventricular pacing at a cycle length of 400 ms under 3 conditions: pacing alone, pacing plus head-up tilt (20 o to 30 o ) to a level that returned cardiac filling pressure to prepacing baseline levels, and pacing plus phenylephrine infusion sufficient to return MAP to prepacing baseline levels. Pacing was sustained for 4 to 5 minutes.…”

Section: Methodsmentioning

confidence: 99%

Reflex Control of Sympathetic Activity During Simulated Ventricular Tachycardia in Humans

et al. 1999

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Background-Ventricular tachyarrhythmias present a unique set of stimuli to arterial and cardiopulmonary baroreceptors by increasing cardiac filling pressures and decreasing arterial pressure. The net effect on the control of sympathetic nerve activity (SNA) in humans is unknown. The purpose of this study was to determine the relative roles of cardiopulmonary and arterial baroreceptors in controlling SNA and arterial pressure during ventricular pacing in humans. Methods and Results-Two experiments were performed in which SNA and hemodynamic responses to ventricular pacing were compared with nitroprusside infusion (NTP) in 12 patients and studied with and without head-up tilt or phenylephrine to normalize the stimuli to either the arterial or cardiopulmonary baroreceptors in 9 patients. In experiment 1, the slope of the relation between SNA and mean arterial pressure was greater during NTP (Ϫ4.7Ϯ1.4 U/mm Hg) than during ventricular pacing (Ϫ3.4Ϯ1.1 U/mm Hg). Comparison of NTP doses and ventricular pacing rates that produced comparable hypotension showed that SNA increased more during NTP (Pϭ0.03). In experiment 2, normalization of arterial pressure during pacing resulted in SNA decreasing below baseline (PϽ0.05), whereas normalization of cardiac filling pressure resulted in a greater increase in SNA than pacing alone (212Ϯ35% versus 189Ϯ37%, Pϭ0.04). Conclusions-These data demonstrate that in humans arterial baroreflex control predominates in mediating sympathoexcitation during ventricular tachyarrhythmias and that cardiopulmonary baroreceptors contribute significant inhibitory modulation. (Circulation. 1999;100:628-634.)

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“…In a similar preparation of canine heart failure, Greenberg et al3 demonstrated decreased sensitivity of atrial type B receptors to volume loading. Zucker et al 4 showed that dogs with heart failure induced by aortocaval fistula had marked attenuation of the sensitivity of medulated left atrial type B receptors to any given change in left atrial pressure. The mechanism for this depressed sensitivity was thought to be due to a decreased left atrial compliance and structural alterations in the neural receptor endings with loss of their normally distinct end-arborizations.…”

Section: Methodsmentioning

confidence: 99%

Selective impairment of baroreflex-mediated vasoconstrictor responses in patients with ventricular dysfunction.

Ferguson¹,

Abboud²,

Mark³

1984

Circulation

226

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The Mechanism of Adaptation of Left Atrial Stretch Receptors in Dogs with Chronic Congestive Heart Failure

Abstract: A B S T R A C T Chronic congestive

Cited by 163 publications

References 48 publications

The neurohumoral and hemodynamic response to orthostatic tilt in patients with congestive heart failure.

The neurohumoral and hemodynamic response to orthostatic tilt in patients with congestive heart failure.

Reflex Control of Sympathetic Activity During Simulated Ventricular Tachycardia in Humans

Selective impairment of baroreflex-mediated vasoconstrictor responses in patients with ventricular dysfunction.

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