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Blood Flow

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Blood is pumped by the heart into the aorta, the largest artery in the body, and then into increasingly smaller arteries, arterioles, and capillaries. The velocity of blood flow decreases with increased cross-sectional blood vessel area. As blood returns to the heart through venules and veins, its velocity increases. The movement of blood is encouraged by smooth muscle in the vessel walls, the movement of skeletal muscle surrounding the vessels, and one-way valves that prevent backflow.

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Related Experiment Video

Updated: Jul 17, 2026

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases

Published on: June 22, 2012

Sickle cell blood flow in the microcirculation.

S A Berger¹, B E Carlson

¹Department of Bioengineering, California University, Berkeley, CA, USA.

Conference Proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference

|February 3, 2007

Summary

Sickle-cell disease causes capillary issues due to deoxygenated red blood cells. Microcirculation models suggest blood pressure may control sickle-cell red blood cell flow.

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Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry

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Published on: November 5, 2019

Area of Science:

Hematology
Biophysics
Medical modeling

Background:

Sickle-cell disease (SCD) involves abnormal red blood cells (RBCs) that cause capillary complications.
Deoxygenation triggers rheological changes in sickle-cell erythrocytes, leading to clinical symptoms and subclinical sequelae.
SCD crises are episodic, painful events linked to microcirculatory dysfunction.

Purpose of the Study:

To model the flow of sickle-cell erythrocytes in capillaries and microcirculatory beds.
To investigate the underlying mechanisms of sickle-cell disease pathophysiology.
To identify potential control parameters in sickle-cell disease microcirculation.

Main Methods:

Development of a computational model for RBC flow in a single capillary, incorporating SCD characteristics.
Extension of the single-capillary model to a pseudo-randomly generated microcirculatory bed.
Analysis of rheological changes in deoxygenated sickle-cell erythrocytes.

Main Results:

The model simulates RBC flow dynamics under deoxygenated conditions.
Simulations reveal potential for abnormal flow events in sickle-cell disease capillaries.
Microcirculatory modeling suggests pressure as a key parameter influencing RBC transit.

Conclusions:

Abnormal capillary events are central to sickle-cell disease symptomology.
Microcirculatory modeling provides insights into SCD pathophysiology.
Blood pressure may be a critical factor regulating sickle-cell red blood cell flow in the microcirculation.