PEG-albumin supraplasma expansion is due to increased vessel wall shear stress induced by blood viscosity shear thinning

Krishna Sriram, Amy G. Tsai, Pedro Cabrales, Fantao Meng, Seetharama A. Acharya, Daniel M. Tartakovsky, Marcos Intaglietta

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

We studied the extreme hemodilution to a hematocrit of 11% induced by three plasma expanders: polyethylene glycol (PEG)-conjugated albumin (PEG-Alb), 6% 70-kDa dextran, and 6% 500-kDa dextran. The experimental component of our study relied on microelectrodes and cardiac output to measure both the rheological properties of plasma-expander blood mixtures and nitric oxide (NO) bioavailability in vessel walls. The modeling component consisted of an analysis of the distribution of wall shear stress (WSS) in the microvessels. Our experiments demonstrated that plasma expansion with PEG-Alb caused a state of supraperfusion with cardiac output 40% above baseline, significantly increased NO vessel wall bioavailability, and lowered peripheral vascular resistance. We attributed this behavior to the shear thinning nature of blood and PEG-Alb mixtures. To substantiate this hypothesis, we developed a mathematical model of non-Newtonian blood flow in a vessel. Our model used the Quemada rheological constitutive relationship to express blood viscosity in terms of both hematocrit and shear rate. The model revealed that the net effect of the hemodilution induced by relatively low-viscosity shear thinning PEG-Alb plasma expanders is to reduce overall blood viscosity and to increase the WSS, thus intensifying endothelial NO production. These changes act synergistically, significantly increasing cardiac output and perfusion due to lowered overall peripheral vascular resistance.

Original languageEnglish (US)
Pages (from-to)2489-2497
Number of pages9
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume302
Issue number12
DOIs
StatePublished - Jun 15 2012

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Blood Viscosity
Vascular Resistance
Albumins
Cardiac Output
Nitric Oxide
Hemodilution
Dextrans
Hematocrit
Biological Availability
Plasma Substitutes
Microelectrodes
Microvessels
Viscosity
Theoretical Models
Perfusion

Keywords

  • Hemodilution
  • Plasma expansion
  • Polyethylene glycol-conjugated albumin
  • Supraperfusion

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine

Cite this

PEG-albumin supraplasma expansion is due to increased vessel wall shear stress induced by blood viscosity shear thinning. / Sriram, Krishna; Tsai, Amy G.; Cabrales, Pedro; Meng, Fantao; Acharya, Seetharama A.; Tartakovsky, Daniel M.; Intaglietta, Marcos.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 302, No. 12, 15.06.2012, p. 2489-2497.

Research output: Contribution to journalArticle

Sriram, Krishna ; Tsai, Amy G. ; Cabrales, Pedro ; Meng, Fantao ; Acharya, Seetharama A. ; Tartakovsky, Daniel M. ; Intaglietta, Marcos. / PEG-albumin supraplasma expansion is due to increased vessel wall shear stress induced by blood viscosity shear thinning. In: American Journal of Physiology - Heart and Circulatory Physiology. 2012 ; Vol. 302, No. 12. pp. 2489-2497.
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