scholarly journals Selective induction of anti-inflammatory monocyte-platelet aggregates in a model of pulsatile blood flow at low shear rates

Platelets ◽  
2016 ◽  
Vol 27 (6) ◽  
pp. 583-592 ◽  
Author(s):  
Yuji Takeda ◽  
Mikio Marumo ◽  
Hidetoshi Nara ◽  
Zhong-Gang Feng ◽  
Hironobu Asao ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulsatile Blood Flow ◽  
Inflammatory Monocyte ◽  
Shear Rates ◽  
Platelet Aggregates ◽  
Anti Inflammatory ◽  
Low Shear

Effect of Blood Viscosity on Thrombosis Potential Near a Step Wall Transition

2009 ◽  
Author(s):  
Scott C. Corbett ◽  
Amin Ajdari ◽  
Ahmet U. Coskun ◽  
Hamid N.-Hashemi
Keyword(s):  
Blood Flow ◽  
Vessel Wall ◽  
Coagulation Factors ◽  
Artificial Organs ◽  
Physical Factors ◽  
Local Geometry ◽  
Induce Platelet Aggregation ◽  
Shear Rates ◽  
Chemical Factors ◽  
Low Shear

Thrombosis and hemolysis are two problems encountered when processing blood in artificial organs. Physical factors of blood flow alone can influence the interaction of proteins and cells with the vessel wall, induce platelet aggregation and influence coagulation factors responsible for the formation of thrombus, even in the absence of chemical factors in the blood. These physical factors are related to the magnitude of the shear rate/stress, the duration of the applied force and the local geometry. Specifically, high blood shear rates (or stress) lead to damage (hemolysis, platelet activation), while low shear rates lead to stagnation and thrombosis [1].

scholarly journals Hydroxyurea Improves Oxygen Transport Effectiveness in Sickle Cell Anemia Patients

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 2716-2716
Author(s):  
Vivien A. Sheehan ◽  
Sheryl Nelson ◽  
Caroline Yappan ◽  
Bogdan R. Dinu ◽  
Danielle Guffey ◽  
...  
Keyword(s):  
Blood Flow ◽  
Sickle Cell ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Patient Characteristics ◽  
Whole Blood Viscosity ◽  
Shear Rates ◽  
High Shear Rates ◽  
Altered Blood ◽  
Low Shear

Abstract Background: Sickle cell disease (SCD) patients have altered blood rheology due to erythrocyte abnormalities, including increased aggregation and reduced deformability, which together affect microcirculatory blood flow and tissue perfusion. At equal hematocrit, sickle cell blood viscosity is increased compared to normal individuals. The hematocrit to viscosity ratio (HVR) is a measure of red blood cell (RBC) oxygen carrying capacity, and is reduced in SCD with clinical consequences related to altered blood flow and reduced tissue oxygenation. Erythrocyte transfusions reduce HVR at low shear rates that mimic venous circulation, and do not change HVR at high shear rates that mimic arterial blood flow. Hydroxyurea is a safe and effective therapy for SCD; however, its effects on sickle cell rheology and HVR have not been fully investigated. Evaluating the effects of hydroxyurea on viscosity is especially critical, before its use is extended widely to patients with cerebrovascular disease or genotypes with higher hematocrit and higher viscosity such as Hemoglobin SC (HbSC). Methods: To determine the effects of hydroxyurea on viscosity and HVR, we designed a prospective study to measure whole blood viscosity at 45 s-1 (low shear) and 225 s-1(high shear) rates in pediatric patients with SCD using a Brookfield cone and plate viscometer under oxygenated conditions. Venous blood samples (1-3mL) were collected in EDTA and analyzed no more than 4 hours after phlebotomy; samples were run in duplicate by persons blinded to the patient’s sickle genotype and treatment status. Laboratory values were obtained using an ADVIA hematology analyzer. Samples were analyzed from three non-overlapping cohorts of patients with SCD and HbAA individuals for comparison: untreated HbSS patients (n= 43), HbSS patients treated with hydroxyurea at maximum tolerated dose (n=98), untreated HbSC patients (n=53) and HbAA patients (n=19). Laboratory parameters that differed significantly among the SCD groups were analyzed by simple linear regression. Results: Patient characteristics and viscosity measurements are shown in the Table. Within the SCD population, the viscosity was lowest among the untreated HbSS patients, presumably due to their low hematocrit, while viscosity was higher in HbSS patients on hydroxyurea and HbSC patients. When the HVR was calculated for each group, no significant difference was identified between untreated HbSS and untreated HbSC patients. However, hydroxyurea treatment significantly increased HVR at both 45s-1 and 225 s-1 (p<0.001), indicating that the slightly increased viscosity in this cohort was more than compensated by a higher hematocrit. Correlations were tested for hemoglobin (Hb), mean corpuscular volume (MCV), white blood cell count (WBC), absolute neutrophil count (ANC), absolute reticulocyte count (ARC), % fetal hemoglobin (HbF), and average red cell density in g/dL with HVR, at both shear rates. The hydroxyurea-associated HVR increase at both shear rates was independent of %HbF or MCV, but the increased HVR at 225 s-1was associated with lower WBC (p<0.001), lower ANC (p=0.002), and lower red cell density (p=.009). Conclusions: We provide prospective data on whole blood viscosity measurements in a large cohort of children with SCD. Hydroxyurea increases the hematocrit in HbSS patients more than the viscosity, and thus improves HVR. These findings imply that hydroxyurea improves RBC oxygen transport at both high and low shear rates, which should confer clinical benefits, and these effects are independent of HbF induction. Concerns about hydroxyurea increasing whole blood viscosity and reducing tissue oxygenation in children with cerebrovascular disease or HbSC patients may not be warranted, if the same beneficial HVR effects are achieved. Abstract 2717. Table 1. Patient characteristics. Viscosity was typically measured in duplicate and averaged for each patient. HVR at 45 s-1 and 225s-1 was calculated as hematocrit/viscosity. Results are presented as mean ± 2SD. HbAAn=19 HbSS, untreatedn=43 HbSS, on Hydroxyurean=98 HbSCn=53 Age (years) 15.4 ± 3.8 10.4 ± 5.1 10.7 ± 3.4 10.5 ± 4.3 Hemoglobin (gm/dL) 13.5 ± 1.7 8.5 ± 1.0 9.9 ± 1.4 11.0 ± 1.2 Hematocrit (%) 40.9 ± 5.3 25.5 ± 3.1 28.4 ± 3.7 31.3 ± 3.2 Viscosity (cP) at 45s-1 5.3 ± 0.9 4.6 ± 1.2 4.3 ± 0.9 5.5 ±0.9 HVR at 45s-1 7.5 ± 0.9 5.8 ± 1.1 6.75 ± 1.0 5.77 ± 0.7 Viscosity (cP) at 225s-1 3.8 ± 0.5 3.3 ± 0.5 3.4 ± 0.5 4.1 ± 0.5 HVR at 225s-1 10.3 ± 0.7 7.7 ± 0.8 8.53 ± 0.8 7.72 ± 0.6 Disclosures Off Label Use: Hydroxyurea is not FDA approved for use in pediatric sickle cell patients.

Numerical simulation of pulsatile blood flow in the human left ventricle

2007 ◽  
Vol 55 (S 1) ◽  
Author(s):  
W Schiller ◽  
K Spiegel ◽  
T Schmid ◽  
H Rudorf ◽  
S Flacke ◽  
...  
Keyword(s):  
Numerical Simulation ◽  
Blood Flow ◽  
Left Ventricle ◽  
Pulsatile Blood Flow ◽  
Human Left Ventricle

scholarly journals Novel Hydrogen Sulfide (H2S)-Releasing BW-HS-101 and Its Non-H2S Releasing Derivative in Modulation of Microscopic and Molecular Parameters of Gastric Mucosal Barrier

2021 ◽  
Vol 22 (10) ◽  
pp. 5211
Author(s):  
Dominik Bakalarz ◽  
Edyta Korbut ◽  
Zhengnan Yuan ◽  
Bingchen Yu ◽  
Dagmara Wójcik ◽  
...  
Keyword(s):  
Blood Flow ◽  
Hydrogen Sulfide ◽  
Gastric Mucosa ◽  
Dna Oxidation ◽  
Gastric Blood Flow ◽  
Gastric Mucosal Damage ◽  
Mucosal Barrier ◽  
Gastric Injury ◽  
Zinc Protoporphyrin ◽  
Anti Inflammatory

Hydrogen sulfide (H2S) is an endogenously produced molecule with anti-inflammatory and cytoprotective properties. We aimed to investigate for the first time if a novel, esterase-sensitive H2S-prodrug, BW-HS-101 with the ability to release H2S in a controllable manner, prevents gastric mucosa against acetylsalicylic acid-induced gastropathy on microscopic and molecular levels. Wistar rats were pretreated intragastrically with vehicle, BW-HS-101 (0.5–50 μmol/kg) or its analogue without the ability to release H2S, BW-iHS-101 prior to ASA administration (125 mg/kg, intragastrically). BW-HS-101 was administered alone or in combination with nitroarginine (L-NNA, 20 mg/kg, intraperitoneally) or zinc protoporphyrin IX (10 mg/kg, intraperitoneally). Gastroprotective effects of BW-HS-101 were additionally evaluated against necrotic damage induced by intragastrical administration of 75% ethanol. Gastric mucosal damage was assessed microscopically, and gastric blood flow was determined by laser flowmetry. Gastric mucosal DNA oxidation and PGE2 concentration were assessed by ELISA. Serum and/or gastric protein concentrations of IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-13, VEGF, GM-CSF, IFN-γ, TNF-α, and EGF were determined by a microbeads/fluorescent-based multiplex assay. Changes in gastric mucosal iNOS, HMOX-1, SOCS3, IL1-R1, IL1-R2, TNF-R2, COX-1, and COX-2 mRNA were assessed by real-time PCR. BW-HS-101 or BW-iHS-101 applied at a dose of 50 μmol/kg protected gastric mucosa against ASA-induced gastric damage and prevented a decrease in the gastric blood flow level. H2S prodrug decreased DNA oxidation, systemic and gastric mucosal inflammation with accompanied upregulation of SOCS3, and EGF and HMOX-1 expression. Pharmacological inhibition of nitric oxide (NO) synthase but not carbon monoxide (CO)/heme oxygenase (HMOX) activity by L-NNA or ZnPP, respectively, reversed the gastroprotective effect of BW-HS-101. BW-HS-101 also protected against ethanol-induced gastric injury formation. We conclude that BW-HS-101, due to its ability to release H2S in a controllable manner, prevents gastric mucosa against drugs-induced gastropathy, inflammation and DNA oxidation, and upregulate gastric microcirculation. Gastroprotective effects of this H2S prodrug involves endogenous NO but not CO activity and could be mediated by cytoprotective and anti-inflammatory SOCS3 and EGF pathways.

Formation and Destruction of Platelet Aggregates in Viscometric Flow

1975 ◽  
Author(s):  
H. Rieger ◽  
H. Schmid-Schönbein
Keyword(s):  
Initial Rate ◽  
Aggregate Stability ◽  
Creeping Flow ◽  
Experimental Conditions ◽  
Shear Rates ◽  
Independent Variables ◽  
Lower Shear ◽  
Platelet Aggregates ◽  
Blood Elements ◽  
Shape Changes

Even after pseudopodia formation platelets - unlike all other known formed blood elements - remain dispersed in stasis and creeping flow and become aggregated only in the presence of a minimum amount of shearing. The “rheoaggregometer” (Rieger et al., Pflüger’s Archiv, 343, R 33, 1973) allows to measure the minimum shear rates necessary for platelet aggregation (PA), as well as the initial rate and the maximum extent of PA in citrated PRP.PA is quantified photometrically as a function of variable shear rates. The initial rate of PA steadily increases with increasing shear rates up to 460 sec-1. However, the maximal extent of PA (indicating the mechanical integrity of formed aggregates) saturates at about 35 sec-1 and then decreases because of a destruction of formed aggregates and of prevention of further PA. The aggregability of the platelets, as reflected by various degrees of shape changes, is enhanced by a drop of temperature and a rise in pH as well as by the so called aggregating agents (e.g. epinephrine 10-6 up to 10-9 M/l) : consecutively lower shear rates (lower effects of collision) are necessary to induce PA. In citrated PRP stable platelet aggregates are produced only within a defined range of shear rates. Platelet aggregability and aggregate stability are independent variables influenced by different experimental conditions.

scholarly journals A Simple Transient Poiseuille-Based Approach to Mimic the Womersley Function and to Model Pulsatile Blood Flow

Dynamics ◽  
2021 ◽  
Vol 1 (1) ◽  
pp. 9-17
Author(s):  
Andrea Natale Impiombato ◽  
Giorgio La Civita ◽  
Francesco Orlandi ◽  
Flavia Schwarz Franceschini Zinani ◽  
Luiz Alberto Oliveira Rocha ◽  
...  
Keyword(s):  
Fluid Dynamics ◽  
Computational Fluid Dynamics ◽  
Blood Flow ◽  
Boundary Conditions ◽  
Quadratic Function ◽  
Pulsatile Blood Flow ◽  
Flow Through ◽  
Simplified Analysis ◽  
Function Models ◽  
Flow Reversals

As it is known, the Womersley function models velocity as a function of radius and time. It has been widely used to simulate the pulsatile blood flow through circular ducts. In this context, the present study is focused on the introduction of a simple function as an approximation of the Womersley function in order to evaluate its accuracy. This approximation consists of a simple quadratic function, suitable to be implemented in most commercial and non-commercial computational fluid dynamics codes, without the aid of external mathematical libraries. The Womersley function and the new function have been implemented here as boundary conditions in OpenFOAM ESI software (v.1906). The discrepancy between the obtained results proved to be within 0.7%, which fully validates the calculation approach implemented here. This approach is valid when a simplified analysis of the system is pointed out, in which flow reversals are not contemplated.

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