The Impact of Erythrocytes Injury on Blood Flow in Bionic Arteriole with Stenosis Segment

Ventricular assist device (VAD) implantation is an effective treatment for patients with end-stage heart failure. However, patients who undergo long-term application of VADs experience a series of VAD-related adverse effects including pump thrombosis, which is induced by rotate impeller-caused blood cell injury and hemolysis. Blood cell trauma-related flow patterns are the key mechanism for understanding thrombus formation. In this study, we established a new method to evaluate the blood cell damage and investigate the real-time characteristics of blood flow patterns in vitro using rheometer and bionic microfluidic devices. The variation of plasma free hemoglobin (PFH) and lactic dehydrogenase (LDH) in the rheometer test showed that high shear stress was the main factor causing erythrocyte membrane injury, while the long-term exposure of high shear stress further aggravated this trauma. Following this rheometer test, the damaged erythrocytes were collected and injected into a bionic microfluidic device. The captured images of bionic microfluidic device tests showed that with the increase of shear stress suffered by the erythrocyte, the migration rate of damaged erythrocyte in bionic microchannel significantly decreased and, meanwhile, aggregation of erythrocyte was clearly observed. Our results indicate that mechanical shear stress caused by erythrocyte injury leads to thrombus formulation and adhesion in arterioles.

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Does High Shear Stress Induced by Blood Flow Lead to Atherosclerosis?

Perspectives in Biology and Medicine ◽

10.1353/pbm.1983.0002 ◽

1983 ◽

Vol 26 (2) ◽

pp. 287-303 ◽

Cited By ~ 19

Author(s):

Margot R. Roach ◽

Norman B. Smith

Keyword(s):

Blood Flow ◽

Shear Stress ◽

High Shear ◽

High Shear Stress

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Hemolysis Caused by Regurgitant Blood Flow With High Shear Stress: An Intractable Complication After Mitral Valve Repair: Reply

The Annals of Thoracic Surgery ◽

10.1016/j.athoracsur.2004.04.073 ◽

2005 ◽

Vol 79 (2) ◽

pp. 754-755

Author(s):

Buu-Khanh Lam ◽

Delos M. Cosgrove ◽

Sunil K. Bhudia ◽

A.Marc Gillinov

Keyword(s):

Blood Flow ◽

Shear Stress ◽

Mitral Valve ◽

Mitral Valve Repair ◽

High Shear ◽

High Shear Stress ◽

Valve Repair

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Nrf2-Keap-1 imbalance under acute shear stress induces inflammatory response in venous endothelial cells

Perfusion ◽

10.1177/02676591211012571 ◽

2021 ◽

pp. 026765912110125

Author(s):

Alexander O Ward ◽

Graciela B Sala-Newby ◽

Shameem Ladak ◽

Gianni D Angelini ◽

Massimo Caputo ◽

...

Keyword(s):

Endothelial Cells ◽

Shear Stress ◽

Target Genes ◽

Nuclear Translocation ◽

Vascular Endothelial Cell ◽

High Shear ◽

High Shear Stress ◽

Protective Environment ◽

The Impact

Vascular endothelial cell stimulation is associated with the activation of different signalling pathways and transcription factors. Acute shear stress is known to induce different pro-inflammatory mediators such as IL-8. Nrf2 is activated by prolonged high shear stress promoting an antiinflammatory and athero-protective environment. However, little is known about the impact of acute shear stress on Nrf2 and Keap1 function and its role in IL-8 regulation. We aimed to examine Nrf2-Keap1 complex activation in-vitro and its role in regulating IL-8 transcripts under acute arterial shear stress (12 dyn/cm2) in venous endothelial cells (ECs). We note that acute high shear stress caused a significant upregulation of Nrf2 target genes, HO-1 and GCLM and an increased IL-8 upregulation at 90 and 120 minutes. Mechanistically, acute high shear did not affect Nrf2 nuclear translocation but resulted in reduced nuclear Keap1, suggesting that the reduction in nuclear Keap1 may result in increased free nuclear nrf2 to induce transcription. Consistently, the suppression of Keap1 using shRNA (shKeap1) resulted in significant upregulation of IL-8 transcripts in response to acute shear stress. Interestingly; the over expression of Nrf2 using Nrf2-Ad-WT or Sulforaphane was also associated with significant upregulation of IL-8 compared to controls. This study highlights the role of Keap1 in Nrf2 activation under shear stress and indicates that activation of Nrf2 may be deleterious in ECs in the context of acute haemodynamic injury.

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Hemolysis Caused by Regurgitant Blood Flow With High Shear Stress: An Intractable Complication After Mitral Valve Repair

The Annals of Thoracic Surgery ◽

10.1016/j.athoracsur.2004.02.151 ◽

2005 ◽

Vol 79 (2) ◽

pp. 754

Author(s):

Shin-ichi Oki ◽

Yoshio Misawa

Keyword(s):

Blood Flow ◽

Shear Stress ◽

Mitral Valve ◽

Mitral Valve Repair ◽

High Shear ◽

High Shear Stress ◽

Valve Repair

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Pulsatility and high shear stress deteriorate barrier phenotype in brain microvascular endothelium

Journal of Cerebral Blood Flow & Metabolism ◽

10.1177/0271678x16672482 ◽

2016 ◽

Vol 37 (7) ◽

pp. 2614-2625 ◽

Cited By ~ 24

Author(s):

Fernando Garcia-Polite ◽

Jordi Martorell ◽

Paula Del Rey-Puech ◽

Pedro Melgar-Lesmes ◽

Caroline C O’Brien ◽

...

Keyword(s):

Endothelial Cells ◽

Shear Stress ◽

Tight Junction ◽

Flow Patterns ◽

Microvascular Endothelial Cells ◽

Brain Microvascular Endothelial Cells ◽

High Shear ◽

High Shear Stress ◽

Microvascular Endothelial ◽

Static Conditions

Microvascular endothelial cells at the blood–brain barrier exhibit a protective phenotype, which is highly induced by biochemical and biomechanical stimuli. Amongst them, shear stress enhances junctional tightness and limits transport at capillary-like levels. Abnormal flow patterns can reduce functional features of macrovascular endothelium. We now examine if this is true in brain microvascular endothelial cells. We suggest in this paper a complex response of endothelial cells to aberrant forces under different flow domains. Human brain microvascular endothelial cells were exposed to physiological or abnormal flow patterns. Physiologic shear (10–20 dyn/cm2) upregulates expression of tight junction markers Zona Occludens 1 (1.7-fold) and Claudin-5 (more than 2-fold). High shear stress (40 dyn/cm2) and/or pulsatility decreased their expression to basal levels and altered junctional morphology. We exposed cells to pathological shear stress patterns followed by capillary-like conditions. Results showed reversible recovery on the expression of tight junction markers. Flow protection of barrier phenotype commensurate with junctional signaling pathways decrease (Src, 0.25-fold, ERK, 0.77-fold) when compared to static conditions. This decrease was lost under high shear and pulsatile flow. In conclusion, abnormal shear stress inherent to systemic vascular disease leads to barrier impairment, which could be reverted by hemodynamic interventions.

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