AJP - Regu Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Regul Integr Comp Physiol 295: R719-R726, 2008. First published July 16, 2008; doi:10.1152/ajpregu.00824.2007
0363-6119/08 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
295/3/R719    most recent
00824.2007v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ramchandra, R.
Right arrow Articles by May, C. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ramchandra, R.
Right arrow Articles by May, C. N.

CALL FOR PAPERS
Physiological and Molecular Mechanisms Implicated in the Neural Control of Circulation

Responses of cardiac sympathetic nerve activity to changes in circulating volume differ in normal and heart failure sheep

Rohit Ramchandra, Sally G. Hood, Anna M. D. Watson, and Clive N. May

Howard Florey Institute, University of Melbourne, Parkville, Australia

Submitted 15 November 2007 ; accepted in final form 12 July 2008

Factors controlling cardiac sympathetic nerve activity (CSNA) in the normal state and those causing the large increase in activity in heart failure (HF) remain unclear. We hypothesized from previous clinical findings that activation of cardiac mechanoreceptors by the increased blood volume in HF may stimulate sympathetic nerve activity (SNA), particularly to the heart via cardiocardiac reflexes. To investigate the effect of volume expansion and depletion on CSNA we have made multiunit recordings of CSNA in conscious normal sheep and sheep paced into HF. In HF sheep (n = 9) compared with normal sheep (n = 9), resting levels of CSNA were significantly higher (34 ± 5 vs. 93 ± 2 bursts/100 heart beats, P < 0.05), mean arterial pressure was lower (76 ± 3 vs. 87 ± 2 mmHg; P < 0.05), and central venous pressure (CVP) was greater (3.0 ± 1.0 vs. 0.0 ± 1.0 mmHg; P < 0.05). In normal sheep (n = 6), hemorrhage (400 ml over 30 min) was associated with a significant increase in CSNA (179 ± 16%) with a decrease in CVP (2.7 ± 0.7 mmHg). Volume expansion (400 ml Gelofusine over 30 min) significantly decreased CSNA (35 ± 12%) and increased CVP (4.7 ± 1.0 mmHg). In HF sheep (n = 6) the responses of CSNA to both volume expansion and hemorrhage were severely blunted with no significant changes in CSNA or heart rate with either stimulus. In summary, these studies in a large conscious mammal demonstrate that in the normal state directly recorded CSNA increased with volume depletion and decreased with volume loading. In contrast, both of these responses were severely blunted in HF with no significant changes in CSNA during either hemorrhage or volume expansion.

heart failure; sympathetic nervous system; hemorrhage; cardiac volume



Address for reprint requests and other correspondence: C. N. May, Howard Florey Institute, Univ. of Melbourne, Parkville, Victoria, 3010, Australia (e-mail: clive.may{at}florey.edu.au)




This article has been cited by other articles:


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
R. Ramchandra, S. G. Hood, R. Frithiof, and C. N. May
Discharge properties of cardiac and renal sympathetic nerves and their impaired responses to changes in blood volume in heart failure
Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2009; 297(3): R665 - R674.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.