Document Detail

Hemodynamic and norepinephrine responses to pacing-induced heart failure in conscious sinoaortic-denervated dogs.
MedLine Citation:
PMID:  8904609     Owner:  NLM     Status:  MEDLINE    
The present study was undertaken to determine the effects of chronic sinoaortic (baroreceptor) denervation (SAD) on the hemodynamic and sympathetic alterations that 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 (prepace) state and each week after the initiation of ventricular pacing at 250 beats/min. After the pacemaker was turned off, hemodynamic and plasma norepinephrine levels returned toward control levels in the prepaced state and after 1 and 2 wk of pacing. However, by 3 wk all hemodynamic and norepinephrine levels remained relatively constant over the 10-min observation period with the pacemaker off. With the pacemaker off, left ventricular end-diastolic pressure went from 2.7 +/- 1.4 (SE) mmHg during the prepace state to 23.2 +/- 2.9 mmHg in the heart failure state in intact dogs (P < 0.01). Left ventricular end-diastolic pressure increased to 27.1 +/- 2.2 mmHg from a control level of 4.2 +/- 1.9 mmHg i 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 beats/min in intact dogs and 136.1 +/- 6.5 beats/min 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 before pacing (197.7 +/- 21.6 vs. 320.6 +/- 26.6 pg/ml; 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 date that the arterial baroreflex is not the sole mechanism for the increase in sympathetic drive in heart failure.
M Brändle; K P Patel; W Wang; I H Zucker
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  81     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  1996 Oct 
Date Detail:
Created Date:  1997-02-19     Completed Date:  1997-02-19     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1855-62     Citation Subset:  IM    
Department of Physiology and Biophysics, University of Nebraska, College of Medicine, Omaha 68198-4575, USA.
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MeSH Terms
Blood Pressure / drug effects,  physiology
Cardiac Pacing, Artificial
Cholinergic Antagonists / pharmacology
Heart Failure / blood,  physiopathology*
Hemodynamics / physiology*
Hexamethonium / pharmacology
Muscle Denervation
Norepinephrine / blood*
Pressoreceptors / drug effects,  physiology
Sinoatrial Node / physiology*
Grant Support
Reg. No./Substance:
0/Cholinergic Antagonists; 51-41-2/Norepinephrine; 60-26-4/Hexamethonium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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