Circulation, Vol 72, 72-81, Copyright © 1985 by American Heart Association
JR Wilson, N Ferraro and DH Wiener
During exercise in patients with heart failure, activation of sympathetic
vasoconstrictor nerves may impair vasodilation in active skeletal muscle
and thereby interfere with skeletal muscle blood flow. To investigate this
hypothesis, we examined the effect of acute alpha- adrenergic blockade with
systemic administration of prazosin (10 patients) or regional
administration of phentolamine (eight patients) on blood flow, vascular
resistance, oxygen consumption (VO2), and lactate release in the leg during
maximal bicycle exercise in patients with heart failure. During control
exercise, systemic VO2 increased to 12.6 +/- 4.3 ml/min/kg (normal greater
than 20 to 25 ml/min/kg), leg blood flow to 2.8 +/- 1.8 liters/min, and leg
lactate release to 362 +/- 256 mg/min. Prazosin decreased systemic vascular
resistance (12.5 +/- 3.2 to 9.7 +/- 2.5 units; p less than .003) and mean
arterial pressure (101 +/- 20 to 87 +/- 22 mm Hg; p less than .002) at
maximal exercise, supporting the presence of substantial sympathetic
vasoconstrictor nerve activity. Prazosin also decreased leg resistance
during exercise. However, the magnitude of leg blood flow, leg oxygen
extraction, and leg VO2 during exercise were unchanged, suggesting that
vasodilation in the leg was produced by an autoregulatory response to the
drop in blood pressure rather than by blockade of sympathetic
vasoconstriction. Maximal systemic VO2 and leg lactate release were also
not improved. Regional blockade with phentolamine did not substantially
drop the arterial blood pressure and had no effect on vasodilation, blood
flow, VO2, and lactate release in the leg during exercise. These data
suggest that during exercise in patients with heart failure, the
sympathetic nervous system helps to sustain arterial blood pressure and
that this beneficial effect is not associated with adverse effects on blood
flow to working skeletal muscle.
ARTICLES
Effect of the sympathetic nervous system on limb circulation and metabolism during exercise in patients with heart failure
This article has been cited by other articles:
![]() |
C. C. Lang, D. B. Chomsky, J. Butler, S. Kapoor, and J. R. Wilson Prostaglandin production contributes to exercise-induced vasodilation in heart failure J Appl Physiol, December 1, 1997; 83(6): 1933 - 1940. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. C. Lang, G. H. Rayos, D. B. Chomsky, A. J. J. Wood, and J. R. Wilson Effect of Sympathoinhibition on Exercise Performance in Patients With Heart Failure Circulation, July 1, 1997; 96(1): 238 - 245. [Abstract] [Full Text] |
||||
![]() |
J. R. Wilson Exercise Intolerance in Heart Failure : Importance of Skeletal Muscle Circulation, January 15, 1995; 91(2): 559 - 561. [Full Text] |
||||
![]() |
J. Myers and V. F. Froelicher Hemodynamic Determinants of Exercise Capacity in Chronic Heart Failure Ann Intern Med, September 1, 1991; 115(5): 377 - 386. [Abstract] [PDF] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1985 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |