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Am J Physiol Regul Integr Comp Physiol (June 15, 2006). doi:10.1152/ajpregu.00212.2006
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Submitted on March 24, 2006
Accepted on June 8, 2006

Abnormal arterial flows by a distributed model of the fetal circulation

Jeroen PHM van den Wijngaard1, Berend E Westerhof2, Dirk J Faber3, Margaret M Ramsay4, Nico Westerhof5, and Martin J. C. Van Gemert1*

1 Laser Center and Department of Obstetrics and Gynecology, Academic Medical Center - University of Amsterdam, Amsterdam, Netherlands
2 BMEYE Cardiovascular Monitoring Company, Academic Medical Center - University of Amsterdam, Amsterdam, Netherlands
3 Laser Center, Academic Medical Center - University of Amsterdam, Amsterdam, Netherlands
4 Department of Obstetrics and Gynecology, Queen's Medical Centre, Nottingham, United Kingdom
5 Laboratory for Physiology, ICaR - VU University Medical Center, Amsterdam, Netherlands

* To whom correspondence should be addressed. E-mail: m.j.vangemert{at}amc.uva.nl.

BACKGROUND: Modeling the propagation of blood pressure and flow along the fetoplacental arterial tree may improve interpretation of abnormal flow velocity waveforms in fetuses. The current models, however, either do not include a wide range of gestational ages, or do not account for variation in anatomical, vascular, or rheological parameters. METHODS: We developed a mathematical model of the pulsating feto-umbilical arterial circulation using Womersley's oscillatory flow theory and viscoelastic arterial wall properties. Arterial flow waves are calculated at different arterial locations from which the pulsatility index (PI) can be determined. We varied blood viscosity, placental and brain resistances, placental compliance, heart rate, stiffness of the arterial wall, and length of the umbilical arteries. RESULTS: The PI increases in the umbilical artery, and decreases in the cerebral arteries, as a result of increasing placental resistance or decreasing brain resistance. Both changes in resistance decrease the flow through the placenta. An increased arterial stiffness increases the PIs in the entire fetoplacental circulation. Blood viscosity and peripheral bed compliance have limited influence on the flow profiles. Bradycardia and tachycardia increase and decrease the PI in all arteries, respectively. Umbilical arterial length has limited influence on the PI but affects the mean arterial pressure at the placental cord insertion. CONCLUSION: The model may improve the interpretation of arterial flow pulsations, and thus may advance both the understanding of pathophysiological processes and clinical management.




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Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
J. P. H. M. van den Wijngaard, B. E. Westerhof, M. G. Ross, and M. J. C. van Gemert
A mathematical model of twin-twin transfusion syndrome with pulsatile arterial circulations
Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2007; 292(4): R1519 - R1531.
[Abstract] [Full Text] [PDF]




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