Baseline arterial pressure affects sympathoexcitatory responses to
ventricular premature beats.
Smith, Michael L., Kenneth A. Ellenbogen, and Dwain L. Eckberg.
Departments of Medicine and Physiology, Hunter Holmes McGuire
Department of Veterans Affairs Medical Center and Medical College of
Virginia, Richmond, Virginia 23249, Current Address: Division of
Cardiology, Case Western Reserve University & University Hospitals
of Cleveland, Cleveland, Ohio 44106
APStracts 2:0121H, 1995.
The seconds to minutes before sudden cardiac death are characterized
by fluctuations of arterial pressure, cardiac rhythm, and probably,
sympathetic nerve activity. We explored the interrelations among
these factors in 7 patients undergoing clinical electrophysiologic
testing. We measured muscle sympathetic nerve activity (SNA) and
arterial pressure responses to ventricular premature beats induced
throughout the cardiac cycle under three conditions: 1) lowered
arterial pressure and elevated SNA produced by intravenous
nitroprusside; 2) baseline arterial pressure and SNA during saline
infusion; and 3) elevated arterial pressure and decreased SNA
activity produced by intravenous phenylephrine. Sympathetic responses
to premature beats were inversely related to diastolic pressure. The
magnitude of the sympathetic response was directly related to the
prevailing arterial pressure and inversely related to baseline SNA.
These data demonstrate that sympathoexcitation evoked by ventricular
dysrhythmias is determined importantly by the prevailing arterial
pressure and possibly by the background R-R interval and level of
sympathetic activity. This effect may influence hemodynamic and
electrophysiologic stability during dysrhythmias.
Received 27 September 1993; accepted in final form 31 January
1995.
APS Manuscript Number H856-3.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 4 April 1995.