Mean arterial pressure nonlinearity in an elastic circulatory system subjected to different hematocrits

Branigan, Tom; Bolster, Diogo; Vázquez, Beatriz Y. Salazar; Intaglietta, Marcos; Tartakovsky, Daniel M.

doi:10.1007/s10237-010-0258-y

Cited by 4 publications

(1 citation statement)

References 18 publications

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“…In previous studies, we modeled the effects of a 10% increase in blood viscosity from baseline and found that it induced a significant decrease in peripheral vascular resistance (8), explaining the in vivo findings of Martini et al (27), who carried the same procedure in unanesthetized hamsters and mice. This effect could be present with 500-kDa dextran extreme hemodilution relative to 70-kDa dextran extreme hemodilution since blood viscosity increases from 2.1 to Fig.…”

Section: Discussionmentioning

confidence: 76%

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

Sriram

Tsai

Cabrales

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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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.

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Section: Discussionmentioning

confidence: 76%

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

Sriram

Tsai

Cabrales

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Hemorheological profiles of subjects with prehypertension

et al. 2016

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High blood viscosity is associated with increased peripheral resistance and high blood pressure (BP). Prehypertension refers to a systemic BP of 120-139 mm Hg systolic (SBP) and/or 80-89 mm Hg diastolic (DBP). Subjects with prehypertension have an increased risk of overt hypertension and incident cardiovascular disease compared with subjects who have optimal BP. In the present study, we investigated the hemorheological profiles of subjects with prehypertension. A total of 418 apparently healthy subjects were enrolled. BP, plasma lipids and glucose were measured using routine methods. Blood and plasma viscosity were measured using a cone-plate viscometer. The participants were grouped according to BP into the following categories: 'normotensive' (n=100), 'prehypertensive' (n=172), and 'hypertensive' (n=146). The blood viscosity, plasma viscosity and hematocrit of the prehypertensive subjects were higher than those of the normotensive subjects (P<0.01), but they were comparable to those of the hypertensive subjects. In simple correlation analyses, SBP and DBP were directly and significantly correlated with age, body mass index (BMI), blood glucose, hematocrit, plasma viscosity and blood viscosity. In multiple regression analyses, age, fasting blood glucose and plasma viscosity were independently related with SBP, whereas blood viscosity, fasting blood glucose and BMI significantly predicted DBP. These data demonstrate that BP in the range of so-called prehypertension is accompanied by important hemorheological changes, which are similar to those observed in people with overt hypertension. These results could explain the increased cardiovascular risk observed in these subjects as well as their susceptibility to hypertension.

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Autoregulation and mechanotransduction control the arteriolar response to small changes in hematocrit

Sriram

Vázquez

Tsai

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Here, we present an analytic model of arteriolar mechanics that accounts for key autoregulation mechanisms, including the myogenic response and the vasodilatory effects of nitric oxide (NO) in the vasculature. It couples the fluid mechanics of blood flow in arterioles with solid mechanics of the vessel wall and includes the effects of wall shear stress- and stretch-induced endothelial NO production. The model can be used to describe the regulation of blood flow and NO transport under small changes in hematocrit and to analyze the regulatory response of arterioles to small changes in hematocrit. Our analysis revealed that the experimentally observed paradoxical increase in cardiac output with small increases in hematocrit results from the combination of increased NO production and the effects of a strong myogenic response modulated by elevated levels of WSS. Our findings support the hypothesis that vascular resistance varies inversely with blood viscosity for small changes in hematocrit in a healthy circulation that responds to shear stress stimuli. They also suggest beneficial effects independent of changes in O(2) carrying capacity associated with the postsurgical transfusion of one or two units of blood.

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Mean arterial pressure nonlinearity in an elastic circulatory system subjected to different hematocrits

Cited by 4 publications

References 18 publications

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

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

Hemorheological profiles of subjects with prehypertension

Autoregulation and mechanotransduction control the arteriolar response to small changes in hematocrit

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