scholarly journals Whole blood viscosity parameters and cerebral blood flow.

Stroke ◽  
1982 ◽  
Vol 13 (3) ◽  
pp. 296-301 ◽  
Author(s):  
J Grotta ◽  
R Ackerman ◽  
J Correia ◽  
G Fallick ◽  
J Chang
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Whole Blood Viscosity

Effect of increased whole blood viscosity on regional blood flows in chronically hypoxemic lambs

1994 ◽  
Vol 267 (2) ◽  
pp. H471-H476
Author(s):  
M. Dalinghaus ◽  
H. Knoester ◽  
J. W. Gratama ◽  
J. Van der Meer ◽  
W. G. Zijlstra ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Oxygen Supply ◽  
Arterial Oxygen ◽  
Organ Blood Flow ◽  
Whole Blood Viscosity ◽  
Blood Flows ◽  
Chronic Hypoxemia

In chronic hypoxemia blood flow and oxygen supply to vital organs are maintained, but to nonvital organs they are decreased. We measured organ blood flows (microspheres) and whole blood viscosity in 10 chronically hypoxemic lambs, with an atrial septal defect and pulmonary stenosis, and in 8 control lambs. Vascular hindrance (resistance/viscosity) was calculated to determine to what extent the effect of increased blood viscosity on organ blood flow was compensated for by a decrease in vascular tone. Arterial oxygen saturation was decreased (68 +/- 10 vs. 91 +/- 3%, P < 0.001), and both hemoglobin concentration (145 +/- 10 vs. 109 +/- 9 g/l, P < 0.05) and blood viscosity (4.4 +/- 0.6 vs. 3.6 +/- 0.6 mPa.s, P < 0.05) were increased in hypoxemic lambs. Systemic blood flow, oxygen supply, oxygen uptake, and blood pressures were not significantly different between hypoxemic and control lambs. Myocardial and cerebral blood flow was maintained in hypoxemic lambs, whereas renal, gastrointestinal, splenic, and thyroidal blood flows were at least 30% lower. Vascular hindrance was significantly decreased in the myocardium and tended to be lower in the brain of hypoxemic lambs, but in all other organs it was similar to that in control lambs. It is concluded that blood flow is redistributed in chronic hypoxemia in lambs; myocardial and cerebral blood flow is maintained, whereas blood flow to splanchnic organs, the kidneys, and the thyroids is decreased. The decreased blood flow to organs is a consequence of the increased whole blood viscosity.

Whole blood viscosity and cerebral blood flow velocities in obese hypertensive or obese normotensive adolescents

2018 ◽  
Vol 31 (3) ◽  
pp. 275-281 ◽  
Author(s):  
Meltem Akcaboy ◽  
Bijen Nazliel ◽  
Tayfun Goktas ◽  
Serdar Kula ◽  
Bülent Celik ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Artery ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Artery Blood Flow ◽  
Whole Blood Viscosity ◽  
Blood Flow Velocities ◽  
Flow Velocities

AbstractBackground:Obesity affects all major organ systems and leads to increased morbidity and mortality. Whole blood viscosity is an important independent regulator of cerebral blood flow. The aim of the present study was to evaluate the effect of whole blood viscosity on cerebral artery blood flow velocities using transcranial Doppler ultrasound in pediatric patients with obesity compared to healthy controls and analyze the effect of whole blood viscosity and blood pressure status to the cerebral artery blood flow velocities.Methods:Sixty patients with obesity diagnosed according to their body mass index (BMI) percentiles aged 13–18 years old were prospectively enrolled. They were grouped as hypertensive or normotensive according to their ambulatory blood pressure monitoring. Whole blood viscosity and middle cerebral artery velocities by transcranial Doppler ultrasound were studied and compared to 20 healthy same aged controls.Results:Whole blood viscosity values in hypertensive (0.0619±0.0077 poise) and normotensive (0.0607±0.0071 poise) groups were higher than controls (0.0616±0.0064 poise), with no significance. Middle cerebral artery blood flow velocities were higher in the obese hypertensive (73.9±15.0 cm/s) and obese normotensive groups (75.2±13.5 cm/s) than controls (66.4±11.5 cm/s), but with no statistical significance.Conclusions:Physiological changes in blood viscosity and changes in blood pressure did not seem to have any direct effect on cerebral blood flow velocities, the reason might be that the cerebral circulation is capable of adaptively modulating itself to changes to maintain a uniform cerebral blood flow.

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.

Abnormal Red Cell Deformability and Aggregation in Sickle Cell Trait

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 1001-1001
Author(s):  
Jon Detterich ◽  
Adam M Bush ◽  
Roberta Miyeko Kato ◽  
Rose Wenby ◽  
Thomas D. Coates ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Red Cell ◽  
Cell Deformability ◽  
Autologous Plasma ◽  
Red Cell Deformability ◽  
Whole Blood Viscosity ◽  
Rbc Aggregation ◽  
Rbc Deformability

Abstract Abstract 1001 Introduction: SCT occurs in 8% of African Americans and is not commonly associated with clinical disease. Nonetheless, the United States Armed Forces has reported that SCT conveys a 30-fold risk of sudden cardiac arrest and a 200-fold risk from exertional rhabdomyolysis. In fact, rhabdomyolysis in athletes with SCT has been the principal cause of death in NCAA football players in the last decade, leading to recently mandated SCT testing in all Division-1 players. In SCT, RBC sickle only under extreme conditions and with slow kinetics. Therefore, rhabdomyolysis most likely occurs in SCT when a “perfect storm” of factors converges to critically imbalance oxygen supply and demand in muscles. We hypothesize that in SCT subjects, abnormal RBC rheology, particularly aggregation and deformability, play an important role in abnormal muscle blood flow supply and distribution to exercising muscle. To test this hypothesis, we examined whole blood viscosity, RBC aggregation, and RBC deformability in 11 SCT and 10 control subjects prior to and following maximum handgrip exercise. Methods: Maximum voluntary contraction (MVC) was assessed by handgrip dynamometer in the dominant arm. Baseline blood was collected for CBC, whole blood viscosity, RBC aggregation, and RBC deformability. Patients then maintained 60% MVC exercise until exhaustion. Following 8 minutes of recovery, a venous blood gas and blood for repeat viscosity assessments was collected from the antecubital fossa of the exercising limb. Whole blood viscosity over a shear rate range of 1–1, 000 1/s was determined by an automated tube viscometer, RBC deformability from 0.5–50 Pa via laser ektacytometry (LORCA) and RBC aggregation in both autologous plasma and 3% dextran 70 kDa using an automated cone-place aggregometer (Myrenne). Aggregation measurements included extent at stasis (M), strength of aggregation (GT min) and kinetics (T ½). Results: Baseline CBC and aggregation values are summarized in Table 1. Both static RBC aggregation in plasma and RBC aggregation in dextran (aggregability) were significantly increased in SCT (Table 1). The rate of aggregation formation trended higher in SCT but the strength of aggregation was not different between the two groups. In SCT subjects, red cell deformability was impaired at low shear stress but greater than controls at higher shear stress (Figure 1). Red cell deformability was completely independent of oxygenation status states in both SCT and control subjects. Whole blood viscosity did not different between the two groups whether oxygenated or deoxygenated and prior to or following handgrip exercise. Discussion: Three important hemorheological differences were observed for SCT subjects versus controls: a) RBC deformability was below control at low stress levels yet greater than control at higher stress; b) The extent of RBC aggregation in autologous plasma was about 40% greater; c) The extent of RBC aggregation for washed RBC re-suspended in an aggregating medium (i.e., 3% dextran 70 kDa) was about 30% higher. RBC deformability is a major determinant of in vivo blood flow dynamics, especially in the microcirculation; decreased deformability adversely affects tissue perfusion. RBC aggregation is also an important determinant since it affects both resistance to blood flow and RBC distribution in a vascular bed (e.g., plasma skimming). The finding of greater aggregability (i.e., higher aggregation in the defined dextran medium) indicates that RBC in SCT have an altered membrane surface in which the penetration of this polymer into the glycocalyx is abnormal. The combined effects of these three rheological parameters is likely to impair in vivo blood flow in SCT, perhaps to a degree resulting in pathophysiological changes of the cardiovascular system. Disclosures: Coates: Novartis: Speakers Bureau; Apopharma: Consultancy. Wood:Ferrokin Biosciences: Consultancy; Shire: Consultancy; Apotex: Consultancy, Honoraria; Novartis: Honoraria, Research Funding.

Plasma viscosity and cerebral blood flow

2000 ◽  
Vol 279 (4) ◽  
pp. H1949-H1954 ◽  
Author(s):  
Yoshinobu Tomiyama ◽  
Johnny E. Brian ◽  
Michael M. Todd
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Viscosity ◽  
Blood Cells ◽  
Exchange Transfusion ◽  
Ringer Solution ◽  
Plasma Viscosity ◽  
High Flow ◽  
Flow Conditions ◽  
Whole Blood Viscosity

We hypothesized that the response of cerebral blood flow (CBF) to changing viscosity would be dependent on “baseline” CBF, with a greater influence of viscosity during high-flow conditions. Plasma viscosity was adjusted to 1.0 or 3.0 cP in rats by exchange transfusion with red blood cells diluted in lactated Ringer solution or with dextran. Cortical CBF was measured by H2 clearance. Two groups of animals remained normoxic and normocarbic and served as controls. Other groups were made anemic, hypercapnic, or hypoxic to increase CBF. Under baseline conditions before intervention, CBF did not differ between groups and averaged 49.4 ± 10.2 ml · 100 g−1 · min−1 (±SD). In control animals, changing plasma viscosity to 1.0 or 3.0 cP resulted in CBF of 55.9 ± 8.6 and 42.5 ± 12.7 ml · 100 g−1 · min−1, respectively (not significant). During hemodilution, hypercapnia, and hypoxia with a plasma viscosity of 1.0 cP, CBF varied from 98 to 115 ml · 100 g−1 · min−1. When plasma viscosity was 3.0 cP during hemodilution, hypercapnia, and hypoxia, CBF ranged from 56 to 58 ml · 100 g−1 · min−1 and was significantly reduced in each case ( P < 0.05). These results support the hypothesis that viscosity has a greater role in regulation of CBF when CBF is increased. In addition, because CBF more closely followed changes in plasma viscosity (rather than whole blood viscosity), we believe that plasma viscosity may be the more important factor in controlling CBF.

scholarly journals Blood Viscoelasticity Response during Carotid Endarterectomy

1992 ◽  
Vol 12 (2) ◽  
pp. 326-333 ◽  
Author(s):  
Michael Hold ◽  
Johann J. Merrelaar ◽  
Peter Hollaus ◽  
Phillipe G. Bull ◽  
Helmuth Denck
Keyword(s):  
Blood Flow ◽  
Carotid Endarterectomy ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Perfusion Pressure ◽  
Complex Viscosity ◽  
Shear Velocity ◽  
Whole Blood Viscosity ◽  
Significant Amelioration ◽  
Microcirculatory Disturbances

As demonstrated in many studies ischemic brain injury causes microcirculatory disturbances which is reflected in changes in the rheological behavior of blood. This is caused by multifactorial interaction between blood cells and damaged endothelium in the capillary network with release of tissue metabolites and byproducts of cellular injury with resulting increased cellular permeability producing a volume shift into the interstitium and, subsequently, a rise in the hematocrit density. Drop in perfusion pressure produces an increase in whole blood viscosity. By means of an oscillating capillary rheometer and densimeter, the viscous and elastic parts of the complex viscosity of whole blood and plasma were measured from the ipsilateral internal jugular vein in 17 patients with unilateral occlusive carotid lesions during different stages of carotid endarterectomy. Our results show that fluid characteristics deteriorated significantly during carotid clamping with increase in whole blood viscoelasticity and plasma density, although collateral circulation was judged sufficient in the angiogram and cerebral perfusion pressure. These parameters not only returned to their initial value, but a significant amelioration was observed after installation of an intraluminal indwelling shunt as a response to improved orthograde flow and an enhanced shear velocity. We conclude that an increase in whole blood viscosity does correlate with decreased cerebral blood flow. This response is immediate. Hematocrit density increases significantly as a result of fluid shift into the interstitium. These changes are reversible if blood flow is promptly restored.

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