Hemodynamic and norepinephrine responses to pacing-induced heart
failure in conscious sino-aortic denervated dogs.
Br[umlaut]andle, Marian, Kaushik P. Patel, Wei Wang, Irving H. Zucker.
Department of Physiology and Biophysics, University of Nebraska
College of Medicine, Omaha, Ne. 68198-4575
APStracts 3:0349A, 1996.
The present study was undertaken to determine the effects of chronic
baroreceptor denervation (SAD) on the hemodynamic and sympathetic
alterations which occur in the pacing-induced model of congestive
heart failure. Two groups of dogs were examined; intact (n=9) and SAD
(n=9). Both groups of dogs were studied in the control (Pre-Pace)
state and each week after the initiation of ventricular pacing at 250
bpm. After turning off the pacemaker, hemodynamics and plasma
norepinephrine levels returned towards control levels in the pre
-paced state and after 1 & 2 weeks of pacing. However, by 3 weeks
all hemodynamic and norepinephrine levels remained relatively
constant over the ten minute observation period with the pacemaker
off. With the pacemaker off, left ventricular end diastolic pressure
(LVEDP) went from 2.7+/-1.4 mm Hg (mean +/- SEM) during the pre-pace
state to 23.2+/-2.9 mm Hg in the heart failure state in intact dogs
(P<.01). LVEDP increased to 27.1+/-2.2 mm Hg from a control of
4.2+/-1.9 mm Hg in SAD dogs (P<0.0003). Mean arterial pressure
significantly decreased in intact and SAD dogs. Resting heart rate
was significantly higher in SAD dogs and increased to 135.8+/-8.9 bpm
in intact dogs and to 136.1+/-6.5 bpm in SAD dogs. There were no
significant differences in the hemodynamic parameters between intact
and SAD dogs after pacing. Plasma norepinephrine was significantly
lower in intact than in SAD dogs prior to pacing (197.7+/-21.6 vs.
320.6+/-26.6 pg/ml, respectively; P<0.005). In the heart failure
state plasma norepinephrine increased significantly in both intact
(598.3+/-44.2 pg/ml) and SAD (644.0+/-64.6 pg/ml) groups. There were
no differences in the severity or the magnitude of the developed
heart failure state in SAD vs. intact dogs. We conclude from these
data that the arterial baroreflex is not the sole mechanism for the
increase in sympathetic drive in heart failure.
Received 21 December 1995; accepted in final form 16 July 1996.
APS Manuscript Number A1335-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 August 1996