Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (998 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The internal resistance of the blood to shear forces. The in vitro measure of whole blood viscosity is of limited clinical utility because it bears little relationship to the actual viscosity within the circulation, but an increase in the viscosity of circulating blood can contribute to morbidity in patients suffering from disorders such as sickle cell anemia and polycythemia.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Blood Viscosities; Viscosities, Blood; Viscosity, Blood.
Where it fits in the MeSH classification
- Broader topics
- Hemorheology
- See also
- Hemorheology
Related concepts
- Blood
- Sickle Cell Anemia
- Polycythemia
Research landscape
PubMed indexes 9,585 records tagged with the MeSH heading “Blood Viscosity” (counts retrieved 2026-10-29). 352 of them (3.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 6,865 records.
Reviews account for 837 records (8.7%) and meta-analyses for 11. Randomized controlled trials number 336 (3.5%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 6,865 |
| 2000-2009 | 1,421 |
| 2010-2019 | 947 |
| 2020 onward | 352 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 837 | 8.7% |
| Meta-analyses | 11 | 0.1% |
| Randomized controlled trials | 336 | 3.5% |
Method: PubMed query "Blood Viscosity"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Red blood cell aggregates and their effect on non-Newtonian blood viscosity at low hematocrit in a two-fluid low shear rate microfluidic system [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Red blood cells (RBCs) are the most abundant cells in human blood.
- Closing excerpt
- Effects of hematocrit, shear rate, viscosity and temperature on RBC aggregate sizes have been quantified.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (323 words)
Red blood cells (RBCs) are the most abundant cells in human blood. Remarkably RBCs deform and bridge together to form aggregates under very low shear rates. The theory and mechanics behind aggregation are, however, not yet completely understood. The main objective of this work is to quantify and characterize RBC aggregates in order to enhance the current understanding of the non-Newtonian behaviour of blood in microcirculation. Suspensions of human blood were flowed and observed in vitro in poly-di-methyl-siloxane (PDMS) microchannels to characterize RBC aggregates. These microchannels were fabricated using standard photolithography methods. Experiments were performed using a micro particle image velocimetry (μPIV) system for shear rate measurements, coupled with a high-speed camera for flow visualization. RBC aggregate sizes were quantified in controlled and measurable shear rate environments for 5, 10 and 15% hematocrit. Aggregate sizes were determined using image processing techniques, while apparent viscosity was measured using optical viscometry. For the samples suspended at 5% H, aggregate size was not strongly correlated with shear rate. For the 10% H suspensions, in contrast, lowering the shear rate below 10 s-1 resulted in a significant increase of RBC aggregate sizes. The viscosity was found to increase with decreasing shear rate and increasing hematocrit, exemplifying the established non-Newtonian shear-thinning behaviour of blood. Increase in aggregation size did not translate into a linear increase of the blood viscosity. Temperature was shown to affect blood viscosity as expected, however, no correlation for aggregate size with temperature was observed. Non-Newtonian parameters associated with power law and Carreau models were determined by fitting the experimental data and can be used towards the simple modeling of blood's non-Newtonian behaviour in microcirculation. This work establishes a relationship between RBC aggregate sizes and corresponding shear rates and one between RBC aggregate sizes and apparent blood viscosity at body and room temperatures, in a microfluidic environment for low hematocrit. Effects of hematocrit, shear rate, viscosity and temperature on RBC aggregate sizes have been quantified.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30024907 · DOI · PMC6053157
Empagliflozin influences blood viscosity and wall shear stress in subjects with type 2 diabetes mellitus compared with incretin-based therapy [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundCardiovascular protection following empagliflozin therapy is not entirely attributable to the glucose lowering effect.
- Closing excerpt
- Furthermore, IMT was markedly reduced early on in the Empagliflozin group.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (193 words)
BackgroundCardiovascular protection following empagliflozin therapy is not entirely attributable to the glucose lowering effect. Increased hematocrit might influence the shear stress that is the main force acting on the endothelium, regulating its anti-atherogenic function.ObjectiveWe designed the study with the aim of investigating the effect of empagliflozin on blood viscosity and shear stress in the carotid arteries. A secondary endpoint was the effect of empagliflozin on carotid artery wall thickness.MethodsThe study was a non-randomized, open, prospective cohort study including 35 type 2 diabetic outpatients who were offered empagliflozin or incretin-based therapy (7 liraglutide, 8 sitagliptin) in combination with insulin and metformin. Blood viscosity, shear stress and carotid wall thickness were measured at baseline and at 1 and 3 months of treatment. Blood viscosity was measured with a viscometer, and shear stress was calculated using a validated formula. Intima-media thickness (IMT) of the carotid artery was detected by ultrasound and was measured with dedicated software.ResultsBlood viscosity (4.87 ± 0.57 vs 5.32 ± 0.66 cP, p ConclusionsThis study is the first to describe a direct effect of empagliflozin on blood viscosity and wall shear stress. Furthermore, IMT was markedly reduced early on in the Empagliflozin group.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29631585 · DOI · PMC5891980
Shear rate specific blood viscosity and shear stress of carotid artery duplex ultrasonography in patients with lacunar infarction [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundThis study describes a new method for determining site-specific vascular shear stress using dynamic measures of shear rate and blood viscosity (BV) in the carotid arteries, and examines characteristics of carotid arterial shear stress among patients with lacunar infarction.
- Closing excerpt
- The use of estimated BV for calculating carotid arterial shear stress provides more accurate assessment of the hemodynamic contribution of shear stress than previous models that have arbitrarily assigned a constant value to this dynamic flow property.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (237 words)
BackgroundThis study describes a new method for determining site-specific vascular shear stress using dynamic measures of shear rate and blood viscosity (BV) in the carotid arteries, and examines characteristics of carotid arterial shear stress among patients with lacunar infarction.MethodsVascular shear stress measurements were conducted in 37 patients (17 lacunar infarction patients and 20 control subjects) using duplex ultrasonography. Vessel wall diameters and velocities were measured in each arterial segment at peak-systolic (PS) and end-diastolic (ED) phases, for calculation of PS/ED shear rates. PS/ED shear stresses [dyne/cm²] were determined with PS/ED shear rates and shear-rate dependent BV values. For comparison, both values of hematocrit-derived BV and BV measurements at 300 s⁻¹ were used for calculation of shear stress.ResultsAll cardiovascular disease (CVD) risk factors including BV values were similar between the two groups. In both common carotid arteries, PS and ED shear stresses were significantly lower in the patients with lacunar infarction than in controls in multivariate models that included age, sex, and other major CVD risk factors. PS and ED shear stresses using the shear rate specific BV were 4.5% lower and 7.3% higher than those using the two other BVs, respectively.ConclusionLacunar infarction was associated with reduced carotid arterial shear stress. The use of estimated BV for calculating carotid arterial shear stress provides more accurate assessment of the hemodynamic contribution of shear stress than previous models that have arbitrarily assigned a constant value to this dynamic flow property.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 23597083 · DOI · PMC3643866
Correlation Between Blood Coagulation Profile and Viscosity: Clinical Laboratory Observational Study [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Whole blood viscosity is a test for blood stasis and is an ideal evidence-based pathology parameter that is largely undervalued and retrogressing in clinical utilization.
- Closing excerpt
- Research may normalize skewed data to obtain better correlation; therefore, further study is required to advance discourse, giving cognizance to clinical practice.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (245 words)
Whole blood viscosity is a test for blood stasis and is an ideal evidence-based pathology parameter that is largely undervalued and retrogressing in clinical utilization. Coagulation profiles as indices of haemostasis are available but limited to central or referral laboratories and often involve long turn-around time. It is therefore important to study the correlation between the index of stasis and indices of haemostasis.ObjectiveTo investigate the correlation of index of stasis with indices of haemostasis.MethodThe clinical laboratory observational research method, using archived pathology data. Indices of haemostasis including activated partial thromboplastin time (APTT) and prothrombin time (PT), the international normalization ratio (INR), and plasma D-dimer were evaluated. On the other hand, the index of blood stasis used was the estimated whole blood viscosity (eWBV) and derived haematocrit and serum protein levels. All (N = 193) tests were collected within a calendar year from the same pathology service, and further, for the correlation, each set of variables from the same blood sample collection was used.ResultsThe haemostasis data are skewed (skewness > 2.0), while eWBV and platelet count are normal (skewness p p ConclusionThere are limitations to the possible correlation between eWBV and haemostasis indices. However, haemostasis indices have inverse associations with eWBV, and the latter can aid in the evaluation of haemostasis hence could be utilized as an alternative or complementary test to haemostasis tests. Research may normalize skewed data to obtain better correlation; therefore, further study is required to advance discourse, giving cognizance to clinical practice.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39982245 · DOI · PMC11843925
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Blood viscosity in tube flow: dependence on diameter and hematocrit [5]
- Research article Vascular wall shear stress: basic principles and methods [6]
- Research article Haematocrit, viscosity, erythrocyte sedimentation rate: meta-analyses of prospective studies of coronary heart disease [7]
- Research article The role of blood rheology in sickle cell disease [8]
- Research article Plasma viscosity: a forgotten variable [9]
- Research article Hypertension, blood viscosity, and cardiovascular morbidity in renal failure: implications of erythropoietin therapy [10]
References
- Mehri R, Mavriplis C, Fenech M. Red blood cell aggregates and their effect on non-Newtonian blood viscosity at low hematocrit in a two-fluid low shear rate microfluidic system. . 2018. PMID 30024907 · DOI · PMC6053157
- Irace C, Casciaro F, Scavelli FB, Oliverio R, Cutruzzolà A, Cortese C, et al.. Empagliflozin influences blood viscosity and wall shear stress in subjects with type 2 diabetes mellitus compared with incretin-based therapy. . 2018. PMID 29631585 · DOI · PMC5891980
- Jeong SK, Rosenson RS. Shear rate specific blood viscosity and shear stress of carotid artery duplex ultrasonography in patients with lacunar infarction. . 2013. PMID 23597083 · DOI · PMC3643866
- Nwose EU, Bwititi PT. Correlation Between Blood Coagulation Profile and Viscosity: Clinical Laboratory Observational Study. . 2025. PMID 39982245 · DOI · PMC11843925
- Pries AR, Neuhaus D, Gaehtgens P. Blood viscosity in tube flow: dependence on diameter and hematocrit. Am J Physiol. 1992. PMID 1481902 · DOI
- Papaioannou TG, Stefanadis C. Vascular wall shear stress: basic principles and methods. Hellenic J Cardiol. 2005. PMID 15807389
- Danesh J, Collins R, Peto R, Lowe GD. Haematocrit, viscosity, erythrocyte sedimentation rate: meta-analyses of prospective studies of coronary heart disease. Eur Heart J. 2000. PMID 10775006 · DOI
- Connes P, Alexy T, Detterich J, Romana M, Hardy-Dessources MD, Ballas SK. The role of blood rheology in sickle cell disease. Blood Rev. 2016. PMID 26341565 · DOI · PMC6447059
- Késmárky G, Kenyeres P, Rábai M, Tóth K. Plasma viscosity: a forgotten variable. Clin Hemorheol Microcirc. 2008. PMID 18503132 · DOI
- Raine AE. Hypertension, blood viscosity, and cardiovascular morbidity in renal failure: implications of erythropoietin therapy. Lancet. 1988. PMID 2891990 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.