Document Detail

Increase in pulse wavelength causes the systemic arterial tree to degenerate into a classical windkessel.
MedLine Citation:
PMID:  17483241     Owner:  NLM     Status:  MEDLINE    
Two competing schools of thought ascribe vascular disease states such as isolated systolic hypertension to fundamentally different arterial system properties. The "windkessel school" describes the arterial system as a compliant chamber that distends and stores blood and relates pulse pressure to total peripheral resistance (R(tot)) and total arterial compliance (C(tot)). Inherent in this description is the assumption that arterial pulse wavelengths are infinite. The "transmission school," assuming a finite pulse wavelength, describes the arterial system as a network of vessels that transmits pulses and relates pulse pressure to the magnitude, timing, and sites of pulse-wave reflection. We hypothesized that the systemic arterial system, described by the transmission school, degenerates into a windkessel when pulse wavelengths increase sufficiently. Parameters affecting pulse wavelength (i.e., heart rate, arterial compliances, and radii) were systematically altered in a realistic, large-scale, human arterial system model, and the resulting pressures were compared with those assuming a classical (2-element) windkessel with the same R(tot) and C(tot). Increasing pulse wavelength as little as 50% (by changing heart rate -33.3%, compliances -55.5%, or radii +50%) caused the distributed arterial system model to degenerate into a classical windkessel (r(2) = 0.99). Model results were validated with analysis of representative human aortic pressure and flow waveforms. Because reported changes in arterial properties with age can markedly increase pulse wavelength, results suggest that isolated systolic hypertension is a manifestation of an arterial system that has degenerated into a windkessel, and thus arterial pressure is a function only of aortic flow, R(tot), and C(tot).
Mohammad W Mohiuddin; Glen A Laine; Christopher M Quick
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2007-05-04
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  293     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2007 Aug 
Date Detail:
Created Date:  2007-08-03     Completed Date:  2007-09-18     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1164-71     Citation Subset:  IM    
Michael E. DeBakey Institute, Texas A&M University, College Station, TX 77843-4466, USA.
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MeSH Terms
Aorta / physiopathology
Arteries / physiopathology*
Blood Pressure*
Bradycardia / physiopathology
Hypertension / physiopathology*
Models, Cardiovascular*
Pulsatile Flow*
Regional Blood Flow
Reproducibility of Results
Time Factors
Vascular Resistance*
Grant Support
620069//PHS HHS; K25 HL70608/HL/NHLBI NIH HHS

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

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