Control of sympathetic nerve activity by vagal mechanoreflexes is blunted in heart failure.
- 1 December 1992
- journal article
- abstracts
- Published by Wolters Kluwer Health in Circulation
- Vol. 86 (6) , 1929-1934
- https://doi.org/10.1161/01.cir.86.6.1929
Abstract
BACKGROUND Previous studies have documented abnormalities of arterial baroreflexes in animals and patients with congestive heart failure. This study determined whether cardiopulmonary reflex control of sympathetic nerve activity was abnormal in a canine model of low-output heart failure induced by rapid ventricular pacing. METHODS AND RESULTS We stimulated mechanoreceptors throughout the cardiopulmonary region by volume expansion and left atrial mechanoreceptors selectively by inflating small balloons at the junctions of the pulmonary veins and left atrium. Responses of renal sympathetic nerve activity and left atrial and systemic arterial pressures were recorded. In the control group, 15% volume expansion raised left atrial pressure 3.5 +/- 0.8 mm Hg and resulted in a 70 +/- 8% reduction in renal nerve activity. In the heart failure group, 15% volume expansion resulted in a 6.8 +/- 3.0 mm Hg rise in left atrial pressure with only a 16 +/- 20% reduction in renal nerve activity (p < 0.01). When volume expansion was performed after pretreatment with hemorrhage to lower left atrial pressure to the normal range in the heart failure group, the markedly attenuated response in the heart failure group persisted. After vagotomy, volume expansion elicited no change in renal nerve activity. Inflation of the atrial balloons caused a 28 +/- 9% reduction in renal sympathetic nerve activity and a 13 +/- 4 mm Hg decrease in arterial pressure in the control group. Renal nerve activity (-5 +/- 3%) and mean arterial pressure (-1 +/- 1 mm Hg) did not change with balloon inflation in the heart failure group. CONCLUSIONS We conclude that dogs with low-output heart failure exhibit marked attenuation of cardiopulmonary mechanoreflex control of sympathetic nerve activity. This attenuated response is mediated via cardiac vagal afferent fibers and is due to either abnormalities in cardiopulmonary baroreceptors or abnormalities in the central nervous system.Keywords
This publication has 18 references indexed in Scilit:
- A Simplified Technique for the Production of Heart Failure in the Dog by Rapid Ventricular PacingThe Lancet Healthy Longevity, 1990
- Neurohumoral and hemodynamic effects of lower body negative pressure in patients with congestive heart failureAmerican Heart Journal, 1989
- Neurohumoral mechanisms involved in congestive heart failureThe American Journal of Cardiology, 1985
- Prostanoids and cardiac reflexes of sympathetic and vagal originThe American Journal of Cardiology, 1983
- Increased plasma arginine vasopressin levels in patients with congestive heart failureJournal of the American College of Cardiology, 1983
- Cardiovascular Afferents Involved in Regulation of Peripheral VesselsAnnual Review of Physiology, 1980
- Plasma norepinephrine in congestive heart failurePublished by Elsevier ,1978
- The Mechanism of Adaptation of Left Atrial Stretch Receptors in Dogs with Chronic Congestive Heart FailureJournal of Clinical Investigation, 1977
- Hemodynamic Effects of Chloralose and Propranolol in DogsActa Physiologica Scandinavica, 1974
- Left ventricular dynamics in dogs during anesthesia with alpha-chloralose and sodium pentobarbitalThe American Journal of Cardiology, 1964