AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 291: H2142-H2151, 2006. First published June 9, 2006; doi:10.1152/ajpheart.00157.2006
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Cascade model of ventricular-arterial coupling and arterial-cardiac baroreflex function for cardiovascular variability in humans

Shigeki Shibata, Rong Zhang, Jeff Hastings, Qi Fu, Kazunobu Okazaki, Ken-ichi Iwasaki, and Benjamin D. Levine

Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, and University of Texas Southwestern Medical Center at Dallas, Dallas, Texas

Submitted 10 February 2006 ; accepted in final form 2 June 2006

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 (R2 = 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.

heart rate variability; blood pressure variability; cardiac mechanics



Address for reprint requests and other correspondence: B. D. Levine, Institute for Exercise and Environmental Medicine, 7232 Greenville Ave, Suite 435, Dallas, TX 75231 (e-mail: benjaminlevine{at}texashealth.org)




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S. Shibata, J. L. Hastings, A. Prasad, Q. Fu, K. Okazaki, M. D. Palmer, R. Zhang, and B. D. Levine
'Dynamic' Starling mechanism: effects of ageing and physical fitness on ventricular-arterial coupling
J. Physiol., April 1, 2008; 586(7): 1951 - 1962.
[Abstract] [Full Text] [PDF]




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