Advanced Constitutive Modeling of the Thixotropic Elasto-Visco-Plastic Behavior of Blood: Steady-State Blood Flow in Microtubes

The present work focuses on the in-silico investigation of the steady-state blood flow in straight microtubes, incorporating advanced constitutive modeling for human blood and blood plasma. The blood constitutive model accounts for the interplay between thixotropy and elasto-visco-plasticity via a scalar variable that describes the level of the local blood structure at any instance. The constitutive model is enhanced by the non-Newtonian modeling of the plasma phase, which features bulk viscoelasticity. Incorporating microcirculation phenomena such as the cell-free layer (CFL) formation or the Fåhraeus and the Fåhraeus-Lindqvist effects is an indispensable part of the blood flow investigation. The coupling between them and the momentum balance is achieved through correlations based on experimental observations. Notably, we propose a new simplified form for the dependence of the apparent viscosity on the hematocrit that predicts the CFL thickness correctly. Our investigation focuses on the impact of the microtube diameter and the pressure-gradient on velocity profiles, normal and shear viscoelastic stresses, and thixotropic properties. We demonstrate the microstructural configuration of blood in steady-state conditions, revealing that blood is highly aggregated in narrow tubes, promoting a flat velocity profile. Additionally, the proper accounting of the CFL thickness shows that for narrow microtubes, the reduction of discharged hematocrit is significant, which in some cases is up to 70%. At high pressure-gradients, the plasmatic proteins in both regions are extended in the flow direction, developing large axial normal stresses, which are more significant in the core region. We also provide normal stress predictions at both the blood/plasma interface (INS) and the tube wall (WNS), which are difficult to measure experimentally. Both decrease with the tube radius; however, they exhibit significant differences in magnitude and type of variation. INS varies linearly from 4.5 to 2 Pa, while WNS exhibits an exponential decrease taking values from 50 mPa to zero.

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Occlusion of Cortical Ascending Venules Causes Blood Flow Decreases, Reversals in Flow Direction, and Vessel Dilation in Upstream Capillaries

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.2011.95 ◽

2011 ◽

Vol 31 (11) ◽

pp. 2243-2254 ◽

Cited By ~ 51

Author(s):

John Nguyen ◽

Nozomi Nishimura ◽

Robert N Fetcho ◽

Costantino Iadecola ◽

Chris B Schaffer

Keyword(s):

Blood Flow ◽

Nearest Neighbor ◽

Flow Direction ◽

Cognitive Disorders ◽

Laser Pulses ◽

Vessel Diameter ◽

Flow Speed ◽

Femtosecond Laser Pulses ◽

Brain Diseases ◽

The Impact

The accumulation of small strokes has been linked to cognitive dysfunction. Although most animal models have focused on the impact of arteriole occlusions, clinical evidence indicates that venule occlusions may also be important. We used two-photon excited fluorescence microscopy to quantify changes in blood flow and vessel diameter in capillaries after occlusion of single ascending or surface cortical venules as a function of the connectivity between the measured capillary and the occluded venule. Clotting was induced by injuring the target vessel wall with femtosecond laser pulses. After an ascending venule (AV) occlusion, upstream capillaries showed decreases in blood flow speed, high rates of reversal in flow direction, and increases in vessel diameter. Surface venule occlusions produced similar effects, unless a collateral venule provided a new drain. Finally, we showed that AVs and penetrating arterioles have different nearest-neighbor spacing but capillaries branching from them have similar topology, which together predicted the severity and spatial extent of blood flow reduction after occlusion of either one. These results provide detailed insights into the widespread hemodynamic changes produced by cortical venule occlusions and may help elucidate the role of venule occlusions in the development of cognitive disorders and other brain diseases.

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Hypoxic cutaneous vasodilation is sustained during brief cold stress and is not affected by changes in CO2

Journal of Applied Physiology ◽

10.1152/japplphysiol.01221.2009 ◽

2010 ◽

Vol 108 (4) ◽

pp. 788-792 ◽

Cited By ~ 12

Author(s):

Grant H. Simmons ◽

Sarah M. Fieger ◽

Christopher T. Minson ◽

John R. Halliwill

Keyword(s):

Blood Flow ◽

Steady State ◽

Cold Stress ◽

Skin Blood Flow ◽

Cold Exposure ◽

Whole Body ◽

Cutaneous Vasodilation ◽

Hypercapnic Hypoxia ◽

Hypoxic Vasodilation ◽

The Impact

Hypoxia decreases core body temperature in animals and humans during cold exposure. In addition, hypoxia increases skin blood flow in thermoneutral conditions, but the impact of hypoxic vasodilation on vasoconstriction during cold exposure is unknown. In this study, skin blood flow was assessed using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC) was calculated as red blood cell flux/mean arterial pressure and normalized to baseline ( n = 7). Subjects were exposed to four different conditions in the steady state (normoxia and poikilocapnic, isocapnic, and hypercapnic hypoxia) and were cooled for 10 min using a water-perfused suit in each condition. CVC increased during all three hypoxic exposures (all P < 0.05 vs. baseline), and the magnitude of these steady-state responses was not affected by changes in end-tidal CO2 levels. During poikilocapnic and hypercapnic hypoxia, cold exposure reduced CVC to the same levels observed during normoxic cooling ( P > 0.05 vs. normoxia), whereas CVC remained elevated throughout cold exposure during isocapnic hypoxia ( P < 0.05 vs. normoxia). The magnitude of vasoconstriction during cold stress was similar in all conditions ( P > 0.05). Thus the magnitude of cutaneous vasodilation during steady-state hypoxia is not affected by CO2 responses. In addition, the magnitude of reflex vasoconstriction is not altered by hypoxia, such that the upward shift in skin blood flow (hypoxic vasodilation) is maintained during whole body cooling.

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1451: Positive Efect of Prostaglandin on Regulation of Prostate Blood Flow-Investigation of the Key Factor in the Signaling Pathway of The Prostate Blood Flow-

The Journal of Urology ◽

10.1016/s0022-5347(18)35585-x ◽

2005 ◽

Vol 173 (4S) ◽

pp. 393-393

Author(s):

Bunzo Kashiwagi ◽

Yasuhiro Shibata ◽

Kazunari Ohki ◽

Seiji Arai ◽

Seijiro Honma ◽

...

Keyword(s):

Blood Flow ◽

Signaling Pathway ◽

Flow Investigation ◽

Key Factor

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Effekt of blood flow shutdown on the vein damage when exposed to HIFU

ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia» ◽

10.25557/0031-2991.2017.02.46-50 ◽

2017 ◽

pp. 46-50

Author(s):

Н.Н. Петрищев ◽

Д.Ю. Семенов ◽

А.Ю. Цибин ◽

Г.Ю. Юкина ◽

А.Е. Беркович ◽

...

Keyword(s):

Blood Flow ◽

Structural Changes ◽

Focused Ultrasound ◽

Vena Cava ◽

Posterior Wall ◽

High Intensity Focused Ultrasound ◽

Vein Wall ◽

Ultrasound Exposure ◽

Isolated Segment ◽

The Impact

The purpose. In the study we investigated the impact of the partial blood flow shutdown on structural changes in the rabbit vena cava posterior wall after exposure to high-intensity focused ultrasound (HIFU). Methods. Ultrasound Exposure: frequency of 1.65 MHz, the ultrasound intensity in the focus of 13.6 kW/cm, the area of the focal spot 1 mm, continuous ultrasound, exposure for 3 seconds. Results. Immediately after HIFU exposure all layers of the vein wall showed characteristic signs of thermal damage. A week after exposure structural changes in the intima, media and adventitia was minimal in the part of vessel with preserved blood flow, and after 4 weeks the changes were not revealed. A week after HIFU exposure partial endothelium destruction, destruction of myocytes, disorganization and consolidation of collagen fibers of the adventitia were observed in an isolated segment of the vessel, and in 4 weeks endothelium restored and signs of damage in media and adventitia persisted, but were less obvious than in a week after exposure. Conclusion. The shutdown of blood flow after exposure to HIFU promotes persistent changes in the vein wall. Vein compression appears to be necessary for the obliteration of the vessel, when using HIFU-technology.

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Anisotropic steady-state creep behavior of Single-crystal β-Sn: A continuum constitutive model based on crystal viscoplasticity

International Journal of Plasticity ◽

10.1016/j.ijplas.2021.102975 ◽

2021 ◽

Vol 140 ◽

pp. 102975

Author(s):

Q. Jiang ◽

A. Dasgupta

Keyword(s):

Steady State ◽

Constitutive Model ◽

Single Crystal ◽

Creep Behavior ◽

Steady State Creep ◽

Model Based

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Independent and combined impact of hypoxia and acute inorganic nitrate ingestion on thermoregulatory responses to the cold

European Journal of Applied Physiology ◽

10.1007/s00421-021-04602-x ◽

2021 ◽

Vol 121 (4) ◽

pp. 1207-1218

Author(s):

Josh T. Arnold ◽

Stephen J. Bailey ◽

Simon G. Hodder ◽

Naoto Fujii ◽

Alex B. Lloyd

Keyword(s):

Blood Flow ◽

Cooling Rate ◽

Skin Blood Flow ◽

Rectal Temperature ◽

Onset Time ◽

Rate Of Change ◽

Vascular Control ◽

Delta Change ◽

Core Cooling ◽

The Impact

Abstract Purpose This study assessed the impact of normobaric hypoxia and acute nitrate ingestion on shivering thermogenesis, cutaneous vascular control, and thermometrics in response to cold stress. Method Eleven male volunteers underwent passive cooling at 10 °C air temperature across four conditions: (1) normoxia with placebo ingestion, (2) hypoxia (0.130 FiO2) with placebo ingestion, (3) normoxia with 13 mmol nitrate ingestion, and (4) hypoxia with nitrate ingestion. Physiological metrics were assessed as a rate of change over 45 min to determine heat loss, and at the point of shivering onset to determine the thermogenic thermoeffector threshold. Result Independently, hypoxia expedited shivering onset time (p = 0.05) due to a faster cooling rate as opposed to a change in central thermoeffector thresholds. Specifically, compared to normoxia, hypoxia increased skin blood flow (p = 0.02), leading to an increased core-cooling rate (p = 0.04) and delta change in rectal temperature (p = 0.03) over 45 min, yet the same rectal temperature at shivering onset (p = 0.9). Independently, nitrate ingestion delayed shivering onset time (p = 0.01), mediated by a change in central thermoeffector thresholds, independent of changes in peripheral heat exchange. Specifically, compared to placebo ingestion, no difference was observed in skin blood flow (p = 0.5), core-cooling rate (p = 0.5), or delta change in rectal temperature (p = 0.7) over 45 min, while nitrate reduced rectal temperature at shivering onset (p = 0.04). No interaction was observed between hypoxia and nitrate ingestion. Conclusion These data improve our understanding of how hypoxia and nitric oxide modulate cold thermoregulation.

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Is there a role for selective vasodilation in the management of sickle cell disease?

Blood ◽

10.1182/blood.v71.3.597.597 ◽

1988 ◽

Vol 71 (3) ◽

pp. 597-602 ◽

Cited By ~ 18

Author(s):

GP Rodgers ◽

MS Roy ◽

CT Noguchi ◽

AN Schechter

Keyword(s):

Blood Flow ◽

Steady State ◽

Sickle Cell Disease ◽

Sickle Cell ◽

Sickle Cell Anemia ◽

Microvascular Obstruction ◽

Controlled Study ◽

Control Group ◽

Cell Disease ◽

Retinal Arteriolar

Abstract To test the hypothesis that microvascular obstruction to blood flow at the level of the arteriole may be significant in individuals with sickle cell anemia, the ophthalmologic effects of orally administered nifedipine were monitored in 11 steady-state patients. Three patients with evidence of acute peripheral retinal arteriolar occlusion displayed a prompt reperfusion of the involved segment. Two other patients showed fading of retroequatorial red retinal lesions. Color vision performance was improved in six of the nine patients tested. The majority of patients also demonstrated a significant decrease in the amount of blanching of the conjunctiva which reflects improved blood flow to this frequently involved area. Such improvements were not observable in a control group of untreated stable sickle cell subjects. These findings support the hypothesis that inappropriate vasoconstriction or frank vasospasm may be a significant factor in the pathogenesis of the microvascular lesions of sickle cell disease and, further, that selective microvascular entrapment inhibition may offer an additional strategy to the management of this disorder. We believe a larger, placebo-controlled study with nifedipine and similar agents is warranted.

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