An artery (plural arteries) (from Greek ἀρτηρία (artēria), meaning 'windpipe, artery')[1] is a blood vessel that takes blood away from the heart to all parts of the body (tissues, lungs, etc). Most arteries carry oxygenated blood; the two exceptions are the pulmonary and the umbilical arteries, which carry deoxygenated blood to the organs that oxygenate it. The effective arterial blood volume is that extracellular fluid which fills the arterial system.

Diagram of an artery
LatinArteria (plural: arteriae)
Anatomical terminology

The arteries are part of the circulatory system, which is responsible for the delivery of oxygen and nutrients to all cells, as well as the removal of carbon dioxide and waste products, the maintenance of optimum blood pH, and the circulation of proteins and cells of the immune system.



Microscopic anatomy of an artery.
Cross-section of a human artery

The anatomy of arteries can be separated into gross anatomy, at the macroscopic level, and microanatomy, which must be studied with a microscope. The arterial system of the human body is divided into systemic arteries, carrying blood from the heart to the whole body, and pulmonary arteries, carrying deoxygenated blood from the heart to the lungs.

The outermost layer of an artery (or vein) is known as the tunica externa, also known as tunica adventitia, and is composed of collagen fibers and elastic tissue - with the largest arteries containing vasa vasorum (small blood vessels that supply large blood vessels)[2]. Most of the layers have a clear boundary between them, however the tunica externa has a boundary that is ill defined. Normally its boundary is considered when it meets or touches the connective tissue.[3] Inside this layer is the tunica media, or media, which is made up of smooth muscle cells, elastic tissue (also called connective tissue proper) and collagen fibres[2]. The innermost layer, which is in direct contact with the flow of blood, is the tunica intima, commonly called the intima. The elastic tissue allows the artery to bend and fit through places in the body. This layer is mainly made up of endothelial cells (and a supporting layer of elastin rich collagen in elastic arteries). The hollow internal cavity in which the blood flows is called the lumen.


Arterial formation begins and ends when endothelial cells begin to express arterial specific genes, such as ephrin B2.[4]


Arteries form part of the human circulatory system

Arteries form part of the circulatory system. They carry blood that is oxygenated after it has been pumped from the heart. Coronary arteries also aid the heart in pumping blood by sending oxygenated blood to the heart, allowing the muscles to function. Arteries carry oxygenated blood away from the heart to the tissues, except for pulmonary arteries, which carry blood to the lungs for oxygenation (usually veins carry deoxygenated blood to the heart but the pulmonary veins carry oxygenated blood as well).[5] There are two types of unique arteries. The pulmonary artery carries blood from the heart to the lungs, where it receives oxygen. It is unique because the blood in it is not "oxygenated", as it has not yet passed through the lungs. The other unique artery is the umbilical artery, which carries deoxygenated blood from a fetus to its mother.

Arteries have a blood pressure higher than other parts of the circulatory system. The pressure in arteries varies during the cardiac cycle. It is highest when the heart contracts and lowest when heart relaxes. The variation in pressure produces a pulse, which can be felt in different areas of the body, such as the radial pulse. Arterioles have the greatest collective influence on both local blood flow and on overall blood pressure. They are the primary "adjustable nozzles" in the blood system, across which the greatest pressure drop occurs. The combination of heart output (cardiac output) and systemic vascular resistance, which refers to the collective resistance of all of the body's arterioles, are the principal determinants of arterial blood pressure at any given moment.

Arteries have the highest pressure and have narrow lumen diameter. It consists of the three tunics: Tunica media, intima and externa.

Systemic arteries are the arteries (including the peripheral arteries), of the systemic circulation, which is the part of the cardiovascular system that carries oxygenated blood away from the heart, to the body, and returns deoxygenated blood back to the heart. Systemic arteries can be subdivided into two types—muscular and elastic—according to the relative compositions of elastic and muscle tissue in their tunica media as well as their size and the makeup of the internal and external elastic lamina. The larger arteries (>10 mm diameter) are generally elastic and the smaller ones (0.1–10 mm) tend to be muscular. Systemic arteries deliver blood to the arterioles, and then to the capillaries, where nutrients and gases are exchanged.

After travelling from the aorta, blood travels through peripheral arteries into smaller arteries called arterioles, and eventually to capillaries. Arterioles help in regulating blood pressure by the variable contraction of the smooth muscle of their walls, and deliver blood to the capillaries.


The aorta is the root systemic artery (i.e., main artery). In humans, it receives blood directly from the left ventricle of the heart via the aortic valve. As the aorta branches, and these arteries branch in turn, they become successively smaller in diameter, down to the arterioles. The arterioles supply capillaries, which in turn empty into venules. The very first branches off of the aorta are the coronary arteries, which supply blood to the heart muscle itself. These are followed by the branches off the aortic arch, namely the brachiocephalic artery, the left common carotid, and the left subclavian arteries.


The capillaries are the smallest of the blood vessels and are part of the microcirculation. The microvessels have a width of a single cell in diameter to aid in the fast and easy diffusion of gases, sugars and nutrients to surrounding tissues. Capillaries have no smooth muscle surrounding them and have a diameter less than that of red blood cells; a red blood cell is typically 7 micrometers outside diameter, capillaries typically 5 micrometers inside diameter. The red blood cells must distort in order to pass through the capillaries.

These small diameters of the capillaries provide a relatively large surface area for the exchange of gases and nutrients.

Clinical significanceEdit

Diagram showing the effects of atherosclerosis on an artery.

Systemic arterial pressures are generated by the forceful contractions of the heart's left ventricle. High blood pressure is a factor in causing arterial damage. Healthy resting arterial pressures are relatively low, mean systemic pressures typically being under 100 mmHg (1.9 psi; 13 kPa) above surrounding atmospheric pressure (about 760 mmHg, 14.7 psi, 101 kPa at sea level). To withstand and adapt to the pressures within, arteries are surrounded by varying thicknesses of smooth muscle which have extensive elastic and inelastic connective tissues. The pulse pressure, being the difference between systolic and diastolic pressure, is determined primarily by the amount of blood ejected by each heart beat, stroke volume, versus the volume and elasticity of the major arteries.

A blood squirt also known as an arterial gush is the effect when an artery is cut due to the higher arterial pressures. Blood is spurted out at a rapid, intermittent rate, that coincides with the heartbeat. The amount of blood loss can be copious, can occur very rapidly, and be life-threatening.[6]

Over time, factors such as elevated arterial blood sugar (particularly as seen in diabetes mellitus), lipoprotein, cholesterol, high blood pressure, stress and smoking, are all implicated in damaging both the endothelium and walls of the arteries, resulting in atherosclerosis. Atherosclerosis is a disease marked by the hardening of arteries. This is caused by an atheroma or plaque in the artery wall and is a build-up of cell debris, that contain lipids, (cholesterol and fatty acids), calcium[7][8] and a variable amount of fibrous connective tissue.

Accidental intraarterial injection either iatrogenically or through recreational drug use can cause symptoms such as intense pain, paresthesia and necrosis. It usually causes permanent damage to the limb; often amputation is necessary.[9]


Among the Ancient Greeks, the arteries were considered to be "air holders" that were responsible for the transport of air to the tissues and were connected to the trachea. This was as a result of finding the arteries of cadavers devoid of blood.

In medieval times, it was recognized that arteries carried a fluid, called "spiritual blood" or "vital spirits", considered to be different from the contents of the veins. This theory went back to Galen. In the late medieval period, the trachea,[10] and ligaments were also called "arteries".[11]

William Harvey described and popularized the modern concept of the circulatory system and the roles of arteries and veins in the 17th century.

Alexis Carrel at the beginning of the 20th century first described the technique for vascular suturing and anastomosis and successfully performed many organ transplantations in animals; he thus actually opened the way to modern vascular surgery that was previously limited to vessels’ permanent ligation.

Theodor Kocher reported that atherosclerosis often developed in patients who had undergone a thyroidectomy and suggested that hypothyroidism favors atherosclerosis, which was, in 1900s autopsies, seen more frequently in iodine-deficient Austrians compared to Icelanders, who are not deficient in iodine. Turner reported the effectiveness of iodide and dried extracts of thyroid in the prevention of atherosclerosis in laboratory rabbits.[12][citation needed]

Arterial Wall Biomechanical CharacterizationEdit

As the heart mechanically pumps the blood flow through the aorta and distributes the blood to all parts of the body, a deeper understanding in the biomechanical interactions between the aortic wall and the blood would further bridge the gap between the progression of an aneurysm and the management of a patient. With a better understanding of an aneurysm development, it is possible to better predict the outcome of the patients by translating the knowledge to clinical settings.

Mechanical loadings including forces, stresses, and deformations are some of the biomechanical factors that would have a more direct influence on aneurysm's progression. To account for the force transfer, the internal wall stress, as well as the structural deformation for biological soft tissue, it is essential to consider how the material composition of tissue would affect the overall tissue properties under various loading conditions. For the case of the aorta, it is understood that each layer consists of various portion of elastin and collagen that provide overall structural support.

The arterial wall consists of three main layers: intima, media, and adventitia. Each layer, separated by elastic lamina, has its own characteristic that provides the overall structural function of the arterial wall. For example, intima primarily provides internal protection of the blood vessel with a smooth endothelial cell layer, elastin, and fibre-reinforced layer. Media, which is considered as transversely isotropic, provides the flexibility to expand and contract under pulsatile blood flow with smooth muscle. Adventitia provides external structural support for the blood vessel with an anisotropic collagen fibre layer. The distribution of microstructures, such as elastin fibres and collagen fibres has been shown to be one of the main contributors that affect the macroscopic biomechanics of arterial wal.

It is well summarized in Tsamis et al. and Back et al. that elastin and collagen content would be affected by age, diseases, genetic or developmental defects including, hypertension, aneurysm, dissection, atherosclerosis, bicuspid aortic valve, Marfan syndrome, and other factors. Specifically for the aortic aneurysm cases, the overall elastin content would decrease withfragmented, disrupted, and irre gular elastin while the overall collagen content would remain the same with thin scattered collagen fibres. The change in elastin and collagen content would result in a less anisotropic aorta. Similarly, for the aortic dissection cases, elastin and collagen concentration also decrease and thus affecting the aorta' s global response to pulsatile pressure. It was also shown that structure integrity would be adversely affected by elastin removal and aneurysm remodeling in the media layer. The tissue toughness of the media layer of the ATAA was shown to be independent of different regions of the aneurysm but depended on both the collagen and elastin fibres.

To further understand the progression of arterial diseases and construct physical models from a biomechanics perspective, it would be necessary to determine the macroscopic material properties of the arterial wall. Recently, many research groups have used uniaxial or biaxial tensile measurements to model the properties of the aortic wall using constitutive equations that account for hyper-elasticity or anisotropy. The characterization of the arterial wall can, therefore, be categorized into isotropic linear elastic material, isotropic hyper-elastic material, and anisotropic hyper-elastic material as discussed in the following sections.

Isotropic linear elastic materialEdit

The constitutive equation of an isotropic elastic material is a simple linear relationship between stress and strain. This relationship is known as Hooke's Law where the given material is characterized by only Young' s modulus and Poisson's ratio. Assuming isothermal condition. Since the strain, or more specifically the engineering strain, used in linear elastic relationship is only valid when deformation is small and within linear range. Therefore, depending on various stress-strain definitions, it is recommended to apply the true (instantaneous changes) stress and true strain relationship for soft tissue experiments.

Fluid-structure interaction (FSI) methods has been used for investigating the arterial wall stress under pulsatile blood flow with an assumption of a linear elastic arterial wall. The assumption of applying isotropic linear elastic material to the arterial wall was made to compensate more relevant global evaluation on aneurysm rupture, asymmetry and wall thickness, stent graft implantation, and multiple arterial layers. Additionally, a uniform aortic wall thickness of a single arterial wall layer could be assumed.

Torii et al. compared the single layer linear elastic and hyper-elastic cerebral aneurysm model and concluded that the hyper-elastic model resulted in a 36% smaller maximum displacement, but with similar displacement patterns, compare with the linear elastic model. To address the rupture risk due to the arterial wall thickness and asymmetry, Scotti et al. found that the non-uniform wall thickness model would result in up to four times greater wall stress, thus increasing AAA rupture risk based on the von Mises failure stress criteria. It is therefore recommended to accurately reproduce the aortic geometry when predicting the biomechanics of aortic aneurysm.

Similarly, Li and Kleistreuer numerically investigated the biomechanics of AAA before and after endovascular stent graft implantation and analyzed the wall stress and aneurysm sac pressure. The use of fully coupled FSI for both AAA and endovascular stent graft resulted in a significant decrease in maximum wall stress for stented AAA when compare with non-stented AAA. The authors also discussed that from their preliminary studies, aneurysm sac pressure and wall stress might increase by 60% with an increase of only 3% endoleak volume as well as a greater endograft drag force from aortic geometrical factors.

Nevertheless, since the arterial wall structure consists of three layers and most biomechanics investigation on aortic aneurysm is modeled as an equivalent single wall layer, Gao et al. considered the multilayer mechanics of arterial wall and analyze stress distribution across each arterial layer. The authors presented an idealized aorta, from the ascending aorta to the descending aorta, (without the aortic branches) with a three-layered aortic wall with a corresponding thickness ratio of 1/6/3 (media thickness of 1.2mm) and isotropic linear elastic properties (Eintima= 2.98 MPa, Emedia = 8.95 MPa, Eadventitia= 2.98 MPa). The circumferential stress was concluded to be directly related to blood pressure resulting in high composite stress around ascending aorta and highest stress at the media layer, suggesting the formation of an aortic dissection.

Applying isotropic linear elastic properties to the aortic wall reduced the modelling complexity while provided an overall macroscopic evaluation on the progression of an aneurysm. However, given the linear elasticity would only be valid within the linear proportional limit, the estimation of the rupture stress for aortic aneurysm would not be accurate as the failure strength is beyond the linear region.

Isotropic hyper-elastic materialEdit

There are several well-established constitutive equations for isotropic hyper-elastic relationship.  The main difference  between  different  relationships, besides the material  constants,  is the method of material properties fittings: exponential  or polynomial.

The material constants used in each constitutive equation are determined experimentally with uniaxial and biaxial tension test using cadaveric, surgical, or animal tissue specimens. The collected data from tensional experiments are usually fitted using multivariable least square analysis. Although the anisotropic material relationship would provide better experimental fit, the use of the neo-Hookean model would be sufficient for describing the material behavior of the media layer.

The characterization of the aortic wall model can be extended to the solid mechanics modeling for multilayer stenotic artery modeling with stent deployment  or modeling the device-wall interaction in coronary sinus. More specifically, Schiavone et al. conducted a finite element simulation on the stent deployment in the stenotic artery using a combination of constitutive equations to model the transcatheter balloon (Mooney-Rivlin 2- parameter), three arterial wall layers, and plaque.

Their simulations suggested that their artery-plaque-stent system would result in significantly different stress distribution with different stent designs. Furthermore, Zahedmanesh and Lally numerically investigated that blood vessel is more likely to get restenosis if the wall stress is greater.

Studies have modelled the arterial wall as a composite of isotropic hyperelastic materials with the material properties derived from experimental studies. However, given that the elastin, collagen fibres and other components in the media and adventitia layer of the aorta affect the deformation and stress distribution of the arterial wall, considering material anisotropy due to collagen fibres when modelling the arterial wall could result in better predictions.

Anisotropic hyper-elastic materialEdit

To further improve the biomechanics model for arterial wall, anisotropy can be added to the isotropic hyper-elastic model. Such an addition will account for the different fibre groups embedded within each arterial wall layer in order to capture the effect of fibre-reinforced deformation in biological soft tissue. Several key studies on the constitutive equations for modeling the anisotropic hyper-elastic arterial wall has been conducted intensively.

To characterize the material constants, several experimental efforts were carried for the modeling of human aorta and the atherosclerotic plaque. Labrosse et al. conducted biaxial and pressurized vessel test for modeling the anisotropic hyper-elastic constitutive equation for human ascending, descending, and abdominal aorta.

See alsoEdit


  1. ^ ἀρτηρία, Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus
  2. ^ a b Steve, Paxton,; Michelle, Peckham,; Adele, Knibbs (2003). "The Leeds Histology Guide". Cite journal requires |journal= (help)CS1 maint: extra punctuation (link)
  3. ^ Sidawy, Anton (2019). Rutherford's Vascular Surgery and Endovascular Therapy. Amsterdam, Netherlands: Elsevier, Inc. pp. 34–48. ISBN 9780323427913.
  4. ^ Swift, MR; Weinstein, BM (Mar 13, 2009). "Arterial-venous specification during development". Circulation Research. 104 (5): 576–88. doi:10.1161/CIRCRESAHA.108.188805. PMID 19286613.
  5. ^ Maton, Anthea; Jean Hopkins; Charles William McLaughlin; Susan Johnson; Maryanna Quon Warner; David LaHart; Jill D. Wright (1999). Human Biology and Health. Englewood Cliffs, New Jersey: Prentice Hall. ISBN 0-13-981176-1.
  6. ^ "U.S. Navy Standard First Aid Manual, Chapter 3 (online)". Retrieved 3 Feb 2003.
  7. ^ Bertazzo, S. et al. Nano-analytical electron microscopy reveals fundamental insights into human cardiovascular tissue calcification. Nature Materials 12, 576-583 (2013).
  8. ^ Miller, J. D. Cardiovascular calcification: Orbicular origins. Nature Materials 12, 476-478 (2013).
  9. ^ Sen MD, Surjya; Nunes Chini MD Phd, Eduardo; Brown MD, Michael J. (June 2005). "Complications After Unintentional Intra-arterial Injection of Drugs: Risks, Outcomes, and Management Strategies" (Online archive of Volume 80, Issue 6, Pages 783–795, June 2005 Mayo Clinic Proceedings). Mayo Clinic Proceedings. MAYO Clinic. Retrieved 25 August 2014. Unintentional intra-arterial injection of medication, either iatrogenic or self-administered, is a source of considerable morbidity. Normal vascular anatomical proximity, aberrant vasculature, procedurally difficult situations, and medical personnel error all contribute to unintentional cannulation of arteries in an attempt to achieve intravenous access. Delivery of certain medications via arterial access has led to clinically important sequelae, including paresthesias, severe pain, motor dysfunction, compartment syndrome, gangrene, and limb loss. We comprehensively review the current literature, highlighting available information on risk factors, symptoms, pathogenesis, sequelae, and management strategies for unintentional intra-arterial injection. We believe that all physicians and ancillary personnel who administer intravenous therapies should be aware of this serious problem.
  10. ^ Oxford English Dictionary.
  11. ^ Shakespeare, William. Hamlet Complete, Authoritative Text with Biographical and Historical Contexts, Critical History, and Essays from Five Contemporary Critical Perspectives. Boston: Bedford Books of St. Martins Press, 1994. pg. 50.
  12. ^ Bruger, Maurice; Rosenkrantz, J. A. (1942-03-01). "Arteriosclerosis and Hypothyroidism: Observations on Their Possible Interrelationship". The Journal of Clinical Endocrinology & Metabolism. 2 (3): 176–180. doi:10.1210/jcem-2-3-176. ISSN 0368-1610.

External linksEdit