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Selective impairment of baroreflex-mediated vasoconstrictor responses in patients with ventricular dysfunction
Journal article   Open access   Peer reviewed

Selective impairment of baroreflex-mediated vasoconstrictor responses in patients with ventricular dysfunction

D. W FERGUSON, F. M ABBOUD and A. L MARK
Circulation (New York, N.Y.), Vol.69(3), pp.451-460
1984
DOI: 10.1161/01.CIR.69.3.451
PMID: 6692507
url
https://doi.org/10.1161/01.CIR.69.3.451View
Published (Version of record) Open Access

Abstract

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 + 0.2 1/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 < .001). During unloading of baroreceptors with LBNP -10 mm Hg, normal subjects developed vasoconstriction (LVRN at LBNP - 10 mm Hg, + 5.7 + 1.6 U) but patients with LVD failed to have vasoconstriction and tended to develop vasodilation (A1FVRLVD 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 at LBNP -40 mm Hg: AFVRN at LBNP -40 mm Hg, + 16.6 + 1.5 U; AFVR at LBNP -40 mm Hg, -10.3 ± 9.6 U (p < .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 < .02). Responses to LBNP tended to be normalized after administration of digitalis glycoside: AFVR during LBNP -40 mm Hg, -11.1 ± 10.5 U before and +7.8 ± 5.6 U after the drug (p < .05). Thus patients with LVD show selective impairment of baroreflex-mediated vasoconstrictor responses to unloading of baroreceptors by simulated orthostatic stress. This does not appear to be caused by high baseline vascular resistance or decreased vascular responsiveness. This response is immediately normalized by administration of a digitalis glycoside, possibly because of baroreceptor sensitization.
 Heart Cardiology. Vascular system Biological and medical sciences Medical sciences Heart failure, cardiogenic pulmonary edema, cardiac enlargement

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