Acute alpha-adrenergic blockade during exercise in heart failure patients decreased systemic vascular resistance (P<0.003) but did not improve leg blood flow, oxygen consumption, or lactate release.
Does acute alpha-adrenergic blockade improve limb circulation and metabolism during exercise in patients with heart failure?
In patients with heart failure, sympathetic nervous system activation during exercise helps sustain arterial blood pressure without adversely affecting blood flow to working skeletal muscle.
Absolute Event Rate: 9.7% vs 12.5%
p-value: p=<0.003
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.
Wilson et al. (Mon,) conducted a other in Heart failure (n=18). Acute alpha-adrenergic blockade (prazosin or phentolamine) vs. Control exercise was evaluated on Systemic vascular resistance at maximal exercise (units) (p=<0.003). Acute alpha-adrenergic blockade during exercise in heart failure patients decreased systemic vascular resistance (P<0.003) but did not improve leg blood flow, oxygen consumption, or lactate release.