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Ferguson DW, Berg WJ, Roach PJ, et al. Effects of heart failure on baroreflex control of sympathetic neural activity. Am J Cardiol. 1992;69(5):523-31doi: 10.1016/0002-9149(92)90998-e.
Ferguson, D. W., Berg, W. J., Roach, P. J., Oren, R. M., & Mark, A. L. (1992). Effects of heart failure on baroreflex control of sympathetic neural activity. The American journal of cardiology, 69(5), 523-31. https://doi.org/10.1016/0002-9149(92)90998-e
Ferguson, D W, et al. "Effects of heart failure on baroreflex control of sympathetic neural activity." The American journal of cardiology vol. 69,5 (1992): 523-31. doi: https://doi.org/10.1016/0002-9149(92)90998-e
Ferguson DW, Berg WJ, Roach PJ, Oren RM, Mark AL. Effects of heart failure on baroreflex control of sympathetic neural activity. Am J Cardiol. 1992 Feb 15;69(5):523-31. doi: 10.1016/0002-9149(92)90998-e. PMID: 1736618.
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Am J Cardiol. 1992 Feb 15;69(5):523-31. doi: 10.1016/0002-9149(92)90998-e.

Effects of heart failure on baroreflex control of sympathetic neural activity.

The American journal of cardiology

D W Ferguson, W J Berg, P J Roach, R M Oren, A L Mark

Affiliations

  1. Department of Internal Medicine, University of Iowa Hospitals, College of Medicine, Iowa City 52242.

PMID: 1736618 DOI: 10.1016/0002-9149(92)90998-e

Abstract

Baroreflex control of heart rate, vascular resistance and norepinephrine is impaired in patients with heart failure, but recent animal studies demonstrate preserved baroreflex control of sympathetic nerve activity in this disorder. Studies were therefore performed to compare baroreflex control of efferent sympathetic nerve activity to muscle in 10 normal subjects (age mean +/- SEM 21 +/- 1 years) and in 11 patients with moderate to severe heart failure (age 48 +/- 5 years, New York Heart Association class II to IV, left ventricular ejection fraction 19 +/- 2%, pulmonary capillary wedge pressure 27 +/- 2 mm Hg, cardiac index 2.04 +/- 0.22 liters/min/m2). Baroreflex activation was produced by intravenous infusion of phenylephrine (0.5 to 2.0 micrograms/kg/min) and deactivation by infusion of nitroprusside (0.4 to 2.5 micrograms/kg/min). During phenylephrine infusion, comparable increases in mean arterial pressure were produced in normal subjects (89 +/- 2 to 99 +/- 3 mm Hg, p less than 0.01) and in patients with heart failure (90 +/- 2 to 99 +/- 3 mm Hg, p less than 0.01). The patients with heart failure exhibited significantly attenuated (p less than 0.01 for normal vs heart failure) decreases in heart rate (93 +/- 5 to 90 +/- 6 beats/min, p = not significant [NS]) compared with normal subjects (67 +/- 3 to 58 +/- 4 beats/min, p less than 0.01) and tended to demonstrate attenuated sympathoinhibitory responses to this pressor stimulus. More strikingly, patients with heart failure demonstrated significant impairment of baroreflex responses during nitroprusside-induced baroreceptor deactivation. In normal subjects, nitroprusside produced a decrease in mean arterial (90 +/- 2 to 80 +/- 3 mm Hg, p less than 0.001) and right atrial (4 +/- 1 to 2 +/- 1 mm Hg, p less than 0.01) pressures with a resultant reflex increase in heart rate (68 +/- 3 to 81 +/- 4 beats/min, p less than 0.001) and muscle sympathetic nerve activity (326 +/- 74 to 746 +/- 147 U/min, p less than 0.01). In patients with heart failure (n = 10), nitroprusside produced comparable (p = NS for normal vs heart failure) decreases in mean arterial (89 +/- 2 to 77 +/- 2 mm Hg, p less than 0.001) and right atrial (6 +/- 1 to 1 +/- 1 mm Hg, p less than 0.001) pressures, but did not significantly alter heart rate (91 +/- 6 to 97 +/- 4 beats/min, p = NS) or sympathetic nerve activity (936 +/- 155 to 1179 +/- 275 U/min, p = NS).(ABSTRACT TRUNCATED AT 400 WORDS)

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