Document Detail

Cascade model of ventricular-arterial coupling and arterial-cardiac baroreflex function for cardiovascular variability in humans.
MedLine Citation:
PMID:  16766646     Owner:  NLM     Status:  MEDLINE    
Cardiovascular variability reflects autonomic regulation of blood pressure (BP) and heart rate (HR). However, systolic BP (SBP) variability also may be induced by fluctuations in stroke volume through left ventricular end-diastolic pressure (LVEDP) variability via dynamic ventricular-arterial coupling during respiration. We hypothesized that dynamic ventricular-arterial coupling is modulated by changes in left ventricular compliance associated with altered preload and that a cascade control mechanism of ventricular-arterial coupling with arterial-cardiac baroreflex function contributes to the genesis of cardiovascular variability at the respiratory frequency. Seven healthy young subjects underwent 6-min recordings of beat-by-beat LVEDP, SBP, and HR in the supine position with controlled respiration at 0.2 Hz during hyper- and hypovolemia. Spectral and transfer function analysis of these variables was conducted between 0.18 and 0.22 Hz. Dynamic ventricular-arterial coupling gain (Gain LVEDP-SBP) was smaller by 25% (P = 0.009) during hypervolemia than during hypovolemia, whereas arterial-cardiac baroreflex function gain (Gain SBP-HR) was similar. As predicted from a cascade model, a linear relationship between Gain LVEDP-HR and LVEDP-SBP times Gain SBP-HR was identified (R(2) = 0.93, P < 0.001). Gain LVEDP-HR was smaller by 40% (P = 0.04) during hypervolemia than during hypovolemia, leading to a reduction in spectral power of HR variability by 45% (P = 0.08). We conclude that dynamic ventricular-arterial coupling gain is reduced during hypervolemia because of a decrease in left ventricular compliance. A cascade model of ventricular-arterial coupling with the arterial-cardiac baroreflex contributes to the genesis of cardiovascular variability at the respiratory frequency.
Shigeki Shibata; Rong Zhang; Jeff Hastings; Qi Fu; Kazunobu Okazaki; Ken-Ichi Iwasaki; Benjamin D Levine
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2006-06-09
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  291     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-10-10     Completed Date:  2007-01-12     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H2142-51     Citation Subset:  IM    
Institute for Exercise and Environmental Medicine, 7232 Greenville Ave, Suite 435, Dallas, TX 75231, USA.
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MeSH Terms
Arteries / physiology*
Autonomic Nervous System / physiology
Baroreflex / physiology*
Blood Pressure / drug effects
Body Mass Index
Cardiovascular Physiological Phenomena*
Cardiovascular System
Diuretics / pharmacology
Furosemide / pharmacology
Heart Rate / drug effects
Models, Cardiovascular
Monitoring, Physiologic
Signal Processing, Computer-Assisted
Stroke Volume
Supine Position
Time Factors
Ventricular Function*
Ventricular Function, Left / physiology*
Grant Support
5R01 AG-01747904/AG/NIA NIH HHS
Reg. No./Substance:
0/Diuretics; 54-31-9/Furosemide

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

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