Circulation, Vol 74, 929-938, Copyright © 1986 by American Heart Association
E Kassis, TN Jacobsen, F Mogensen and O Amtorp
Mechanisms controlling forearm muscle vascular resistance (FMVR) during
postural changes were investigated in seven patients with severe congestive
heart failure (CHF) and in seven control subjects with unimpaired left
ventricular function. Relative brachioradial muscle blood flow was
determined by the local 133Xe-washout technique. Unloading of baroreceptors
with use of 45 degree upright tilt was comparably obtained in the patients
with CHF and control subjects. Control subjects had substantially increased
FMVR and heart rate to maintain arterial pressure whereas patients with CHF
had decreased FMVR by 51 +/- 11% (mean +/- SEM, p less than .02) and had no
increase in heart rate despite a fall in arterial pressure during upright
tilt. The autoregulatory and local vasoconstrictor reflex responsiveness
during postural changes in forearm vascular pressures were intact in both
groups. Further investigations were carried out in the patients with CHF.
The left axillary nerve plexus was blocked by local anesthesia in the seven
patients. No alterations in forearm vascular pressures were observed. This
blockade preserved the local regulation of FMVR but reversed the
vasodilator response to upright tilt as FMVR increased by 30 +/- 7% (p less
than .02). Blockade of central neural impulses to this limb combined with
brachial arterial infusions of phentolamine completely abolished the
humoral vasoconstriction in the tilted position. Infusions of propranolol
to the contralateral brachial artery that did not affect baseline values of
heart rate, arterial pressure, or the local reflex regulation of FMVR
reversed the abnormal vasodilator response to upright tilt as FMVR
increased by 42 +/- 12% (p less than .02). Despite augmented baseline
values, forearm venous but not arterial plasma levels of epinephrine
increased in the tilted position, as did arterial rather than venous plasma
concentrations of norepinephrine in these patients. The results suggest a
beta-adrenergic reflex mechanism elicited by spinal or supraspinal neural
impulses and probably modulating a cotransmitter release in the patients
with CHF.
ARTICLES
Sympathetic reflex control of skeletal muscle blood flow in patients with congestive heart failure: evidence for beta-adrenergic circulatory control
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