Circulation, Vol 69, 451-460, Copyright © 1984 by American Heart Association
DW Ferguson, FM Abboud and AL Mark
Cardiac dysfunction in animals has been associated with impairment of
arterial and cardiopulmonary baroreflex control of the circulation. Chronic
heart failure in human beings is associated with neurohumoral excitation,
which could result in part from impairment in the inhibitory influence of
baroreflexes. We postulated that (1) patients with left ventricular
dysfunction (LVD) have impaired baroreflex modulation of vascular
resistance and (2) administration of a digitalis glycoside would
immediately restore baroreflex sensitivity. Eleven patients with LVD (NYHA
class, 2.8 +/- 0.2, mean +/- SEM; baseline left ventricular ejection
fraction, 18 +/- 2%; cardiac index, 2.4 +/- 0.21/min/m2; and pulmonary
capillary wedge pressure, 26.0 +/- 3.2 mm Hg) were compared with 17 normal
control subjects. We measured forearm vasoconstrictor responses to
simulated orthostatic stress with use of lower body negative pressure
(LBNP) at -10 and -40 mm Hg to unload cardiopulmonary and arterial
baroreceptors. Baseline forearm vascular resistance (FVR) was higher in
patients with LVD than in normal subjects: FVRLVD, 68.8 +/- 15.3 U; FVRN,
23.2 +/- 2.1 U (p less than .001). During unloading of baroreceptors with
LBNP -10 mm Hg, normal subjects developed vasoconstriction (delta VRN at
LBNP -10 mm Hg, +5.7 +/- 1.6 U) but patients with LVD failed to have
vasoconstriction and tended to develop vasodilation (delta FVRLVD at LBNP
-10 mm Hg, -8.6 +/- 8.5 U) (p = .05, normals vs patients with LVD at LBNP
-10 mm Hg). A more marked disparity in response was seen during unloading
of baroreceptors of LBNP -40 mm Hg: delta FVRN at LBNP -40 mm Hg, +16.6 +/-
1.5 U; delta FVRLVD at LBNP -40 mm Hg, -10.3 +/- 9.6 U (p less than .001,
normals vs patients with LVD). Despite high baseline values for FVR,
patients with LVD developed vasoconstriction during intra-arterial
infusions of norepinephrine, thereby excluding a nonspecific depression of
vascular reactivity as the mechanism for abnormal responses to LBNP in
patients with LVD. We also studied the short-term effects of administration
of a digitalis glycoside, ouabain 0.0075 mg/kg (seven patients) or
lanatoside C (Cedilanid-D) 0.02 mg/kg (three patients), on
baroreflex-mediated vasoconstrictor responses to LBNP in the patients with
LVD. Digitalis glycoside reduced baseline FVR from 71.8 +/- 16.6 to 48.6
+/- 12.0 U (p less than .02). Responses to LBNP tended to be normalized
after administration of digitalis glycoside: delta FVR during LBNP -40 mm
Hg, -11.1 +/- 10.5 U before and +7.8 +/- 5.6 U after the drug (p less than
.05).(ABSTRACT TRUNCATED AT 400 WORDS)
ARTICLES
Selective impairment of baroreflex-mediated vasoconstrictor responses in patients with ventricular dysfunction
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