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Blood vessel

For other uses, see Blood vessel (disambiguation).
Blood vessel
Diagram blood vessels
Details
SystemCirculatory system
Identifiers
Latinvas sanguineum
MeSHD001808
TA98A12.0.00.001
TA23895
FMA63183
Anatomical terminology

Blood vessels are the tubular structures of a circulatory system that transport blood throughout a vertebrate's body.[1] Blood vessels transport blood cells, nutrients, and oxygen to most of the tissues of a body. They also take waste and carbon dioxide away from the tissues.[2] Some tissues such as cartilage, epithelium, and the lens and cornea of the eye are not supplied with blood vessels and are termed avascular.

There are five types of blood vessels: the arteries, which carry the blood away from the heart; the arterioles; the capillaries, where the exchange of water and chemicals between the blood and the tissues occurs; the venules; and the veins, which carry blood from the capillaries back towards the heart.

The word vascular, is derived from the Latin vas, meaning vessel, and is mostly used in relation to blood vessels.

Etymology

  • artery – late Middle English; from Latin arteria, from Greek artēria, probably from airein ("raise").[3]
  • vein – Middle English; from Old French veine, from Latin vena.[4]
  • capillary – mid-17th century; from Latin capillaris, from capillus ("hair"), influenced by Old French capillaire.[5]

Structure

The arteries and veins have three layers. The middle layer is thicker in the arteries than it is in the veins:[6]

  • The inner layer, tunica intima, is the thinnest layer. It is a single layer of flat cells (simple squamous epithelium) glued by a polysaccharide intercellular matrix, surrounded by a thin layer of subendothelial connective tissue interlaced with a number of circularly arranged elastic bands called the internal elastic lamina. A thin membrane of elastic fibers in the tunica intima run parallel to the vessel.
  • The middle layer of tunica media is the thickest layer in arteries. It consists of circularly arranged elastic fiber, connective tissue and polysaccharide substances; the second and third layer are separated by another thick elastic band called external elastic lamina.[7] The tunica media may (especially in arteries) be rich in vascular smooth muscle, which controls the caliber of the vessel. Veins do not have the external elastic lamina, but only an internal one. The tunica media is thicker in the arteries rather than the veins.
  • The outer layer is the tunica adventitia and the thickest layer in veins. It is entirely made of connective tissue. It also contains nerves that supply the vessel as well as nutrient capillaries (vasa vasorum) in the larger blood vessels.

Capillaries consist of a single layer of endothelial cells with a supporting subendothelium consisting of a basement membrane and connective tissue. When blood vessels connect to form a region of diffuse vascular supply, it is called an anastomosis. Anastomoses provide alternative routes for blood to flow through in case of blockages. Veins can have valves that prevent the backflow of the blood that was being pumped against gravity by the surrounding muscles.[8] In humans, arteries do not have valves except for the two 'arteries' that originate from the heart's ventricles.[9]

Early estimates by Danish physiologist August Krogh suggested that the total length of capillaries in human muscles could reach approximately 100,000 kilometres (62,000 mi). (assuming an ideal human body, like that of a bodybuilder)[10] However, later studies suggest a more conservative figure of 9,000–19,000 kilometres (5,600–11,800 mi) taking into account updated capillary density and average muscle mass in adults.[11] Despite these later studies, many textbooks or other types of media include Krogh's estimates as a fun fact as opposed to the more recent studies.[12][better source needed]

Types

There are various kinds of blood vessels:[13]

They are roughly grouped as "arterial" and "venous", determined by whether the blood in it is flowing away from (arterial) or toward (venous) the heart. The term "arterial blood" is nevertheless used to indicate blood high in oxygen, although the pulmonary artery carries "venous blood" and blood flowing in the pulmonary vein is rich in oxygen. This is because they are carrying the blood to and from the lungs, respectively, to be oxygenated.[citation needed]

Function

See also: Circulatory system

Blood vessels function to transport blood to an animal's body tissues. In general, arteries and arterioles transport oxygenated blood from the lungs to the body and its organs, and veins and venules transport deoxygenated blood from the body to the lungs. Blood vessels also circulate blood throughout the circulatory system. Oxygen (bound to hemoglobin in red blood cells) is the most critical nutrient carried by the blood. In all arteries apart from the pulmonary artery, hemoglobin is highly saturated (95–100%) with oxygen. In all veins, apart from the pulmonary vein, the saturation of hemoglobin is about 75%.[14][15] (The values are reversed in the pulmonary circulation.) In addition to carrying oxygen, blood also carries hormones, and nutrients to the cells of a body and removes waste products.[16]

Blood vessels do not actively engage in the transport of blood (they have no appreciable peristalsis). Blood is propelled through arteries and arterioles through pressure generated by the heartbeat.[17] Blood vessels also transport red blood cells. Hematocrit tests can be performed to calculate the proportion of red blood cells in the blood. Higher proportions result in conditions such as dehydration or heart disease, while lower proportions could lead to anemia and long-term blood loss.[18]

Permeability of the endothelium is pivotal in the release of nutrients to the tissue. It is also increased in inflammation in response to histamine,[19] prostaglandins[20] and interleukins,[21] which leads to most of the symptoms of inflammation (swelling, redness, warmth and pain).

Constriction

Main article: Vasoconstriction
Transmission electron micrograph of a microvessel displaying an erythrocyte (E) within its lumen which is deformed due to vasoconstriction

Arteries—and veins to a degree—can regulate their inner diameter by contraction of the muscular layer. This changes the blood flow to downstream organs and is determined by the autonomic nervous system. Vasodilation and vasoconstriction are also used antagonistically as methods of thermoregulation.[22]

The size of blood vessels is different for each of them. It ranges from a diameter of about 30–25 millimeters for the aorta[23] to only about 5 micrometers (0,005 mm) for the capillaries.[24] Vasoconstriction is the constriction of blood vessels (narrowing, becoming smaller in cross-sectional area) by contracting the vascular smooth muscle in the vessel walls. It is regulated by vasoconstrictors (agents that cause vasoconstriction). These can include paracrine factors (e.g., prostaglandins), a number of hormones (e.g., vasopressin and angiotensin[25]) and neurotransmitters (e.g., epinephrine) from the nervous system.

Vasodilation is a similar process mediated by antagonistically acting mediators. The most prominent vasodilator is nitric oxide (termed endothelium-derived relaxing factor for this reason).[26]

Flow

Main article: Vascular resistance

The circulatory system uses the channel of blood vessels to deliver blood to all parts of the body. This is a result of the left and right sides of the heart working together to allow blood to flow continuously to the lungs and other parts of the body. Oxygen-poor blood enters the right side of the heart through two large veins. Oxygen-rich blood from the lungs enters through the pulmonary veins on the left side of the heart into the aorta and then reaches the rest of the body. The capillaries are responsible for allowing the blood to receive oxygen through tiny air sacs in the lungs. This is also the site where carbon dioxide exits the blood. This all occurs in the lungs where blood is oxygenated.[27]

The blood pressure in blood vessels is traditionally expressed in millimetres of mercury (1 mmHg = 133 Pa). In the arterial system, this is usually around 120 mmHg systolic (high pressure wave due to contraction of the heart) and 80 mmHg diastolic (low pressure wave). In contrast, pressures in the venous system are constant and rarely exceed 10 mmHg.[28]

Vascular resistance occurs when the vessels away from the heart oppose the flow of blood. Resistance is an accumulation of three different factors: blood viscosity, blood vessel length and vessel radius.[29] Blood viscosity is the thickness of the blood and its resistance to flow as a result of the different components of the blood. Blood is 92% water by weight and the rest of blood is composed of protein, nutrients, electrolytes, wastes, and dissolved gases. Depending on the health of an individual, the blood viscosity can vary (i.e., anemia causing relatively lower concentrations of protein, high blood pressure an increase in dissolved salts or lipids, etc.).[29]

Vessel length is the total length of the vessel measured as the distance away from the heart. As the total length of the vessel increases, the total resistance as a result of friction will increase.[29] Vessel radius also affects the total resistance as a result of contact with the vessel wall. As the radius of the wall gets smaller, the proportion of the blood making contact with the wall will increase. The greater amount of contact with the wall will increase the total resistance against the blood flow.[30]

Disease

Main article: Vascular disease

Blood vessels play a huge role in virtually every medical condition. Cancer, for example, cannot progress unless the tumor causes angiogenesis (formation of new blood vessels) to supply the malignant cells' metabolic demand.[31] Atherosclerosis represents around 85% of all deaths from cardiovascular diseases due to the buildup of plaque.[32] Coronary artery disease that often follows after atherosclerosis can cause heart attacks or cardiac arrest, resulting in 370,000 worldwide deaths in 2022.[33] In 2019, around 17.9 million people died from cardiovascular diseases. Of these deaths, around 85% of them were due to heart attack and stroke.[34]

Blood vessel permeability is increased in inflammation. Damage, due to trauma or spontaneously, may lead to hemorrhage due to mechanical damage to the vessel endothelium. In contrast, occlusion of the blood vessel by atherosclerotic plaque, an embolised blood clot or a foreign body leads to downstream ischemia (insufficient blood supply) and possibly infarction (necrosis due to lack of blood supply). Vessel occlusion tends to be a positive feedback system; an occluded vessel creates eddies in the normally laminar flow or plug flow blood currents. These eddies create abnormal fluid velocity gradients which push blood elements, such as cholesterol or chylomicron bodies, to the endothelium. These deposit onto the arterial walls which are already partially occluded and build upon the blockage.[35]

The most common disease of the blood vessels is hypertension or high blood pressure. This is caused by an increase in the pressure of the blood flowing through the vessels. Hypertension can lead to heart failure and stroke. Aspirin helps prevent blood clots and can also help limit inflammation.[36] Vasculitis is inflammation of the vessel wall due to autoimmune disease or infection.

References

  1. ^ Shea MJ. "Blood Vessels – Heart and Blood Vessel Disorders". Merck Manuals Consumer Version. Merck Sharp & Dohme Corp. Archived from the original on April 24, 2015. Retrieved December 22, 2016.
  2. ^ "How Does Blood Flow Through Your Body". Cleveland Clinic.
  3. ^ "artery, noun". Oxford Learner's Dictionaries. Word Origin.
  4. ^ "Middle English Dictionary Entry of vein and veine". Middle English Compendium.
  5. ^ "capillary, noun". Oxford Learner's Dictionaries. Word Origin.
  6. ^ Taylor AM, Bordoni B (2024), "Histology, Blood Vascular System", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 31985998, retrieved April 7, 2024
  7. ^ Qin G, Wang L, Hua Y, et al. (April 1, 2020). "Comparative morphology of the internal elastic lamina of cerebral and peripheral arteries". International Journal of Clinical and Experimental Pathology. 13 (4): 764–770. PMC 7191140. PMID 32355525.
  8. ^ D Douketis J (2023). "Overview of the Venous System". MSD Manual.
  9. ^ The exception is the pulmonary artery and the aorta.
  10. ^ Krogh A (1922). The anatomy and physiology of capillaries. Gerstein - University of Toronto. New Haven, Yale Univ. Press.
  11. ^ Poole DC, Kano Y, Koga S, et al. (2021). "August Krogh: Muscle capillary function and oxygen delivery". Comparative Biochemistry and Physiology. Part A, Molecular & Integrative Physiology. 253: 110852. doi:10.1016/j.cbpa.2020.110852. ISSN 1531-4332. PMC 7867635. PMID 33242636.
  12. ^ Kurzgesagt – In a Nutshell (October 29, 2024). We Fell For The Oldest Lie On The Internet. Retrieved November 20, 2024 – via YouTube.
  13. ^ Tucker WD, Arora Y, Mahajan K (2024), "Anatomy, Blood Vessels", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 29262226, retrieved April 17, 2024
  14. ^ "Central Venous/Mixed Venous Oxygen Saturation". London Health Sciences Centre. London, Ontario, CA. Retrieved August 8, 2021.
  15. ^ "Hypoxemia (low blood oxygen)". Mayo Clinic. Retrieved August 8, 2021.
  16. ^ Prisby RD (August 16, 2017). "Mechanical, hormonal and metabolic influences on blood vessels, blood flow and bone". The Journal of Endocrinology. 235 (3): R77–R100. doi:10.1530/JOE-16-0666. PMC 5611884. PMID 28814440.
  17. ^ Khan MG (2006). "Anatomy of the Heart and Circulation". Encyclopedia of Heart Disease. Amsterdam: Academic Press. pp. 13–22. ISBN 978-0-08-045481-8.
  18. ^ "Hematocrit test – Mayo Clinic". www.mayoclinic.org.
  19. ^ Ashina K, Tsubosaka Y, Nakamura T, et al. (2015). "Histamine Induces Vascular Hyperpermeability by Increasing Blood Flow and Endothelial Barrier Disruption In Vivo". PLOS ONE. 10 (7): e0132367. doi:10.1371/journal.pone.0132367. ISSN 1932-6203. PMC 4497677. PMID 26158531.
  20. ^ Rittchen S, Rohrer K, Platzer W, et al. (December 1, 2020). "Prostaglandin D2 strengthens human endothelial barrier by activation of E-type receptor 4". Biochemical Pharmacology. 182: 114277. doi:10.1016/j.bcp.2020.114277. ISSN 0006-2952. PMID 33038299.
  21. ^ Yu H, Huang X, Ma Y, et al. (2013). "Interleukin-8 regulates endothelial permeability by down-regulation of tight junction but not dependent on integrins induced focal adhesions". International Journal of Biological Sciences. 9 (9): 966–979. doi:10.7150/ijbs.6996. ISSN 1449-2288. PMC 3805902. PMID 24155670.
  22. ^ Charkoudian N (October 2010). "Mechanisms and modifiers of reflex induced cutaneous vasodilation and vasoconstriction in humans". Journal of Applied Physiology. 109 (4): 1221–1228. doi:10.1152/japplphysiol.00298.2010. PMC 2963327. PMID 20448028.
  23. ^ Erbel R, Eggebrecht H (2006). "Aortic dimensions and the risk of dissection". Heart. 92 (1): 137–142. doi:10.1136/hrt.2004.055111. PMC 1861012. PMID 16365370. The normal diameter of the abdominal aorta is regarded to be less than 3.0 cm.
  24. ^ Potter RF, Groom AC (1983). "Capillary diameter and geometry in cardiac and skeletal muscle studied by means of corrosion casts". Microvascular Research. 25 (1): 68–84. doi:10.1016/0026-2862(83)90044-4. ISSN 0026-2862. PMID 6835100.
  25. ^ Kanaide H, Ichiki T, Nishimura J, et al. (November 28, 2003). "Cellular Mechanism of Vasoconstriction Induced by Angiotensin II". Circulation Research. 93 (11): 1015–1017. doi:10.1161/01.res.0000105920.33926.60. ISSN 0009-7330. PMID 14645130.
  26. ^ Cooke JP (2000). "The endothelium: a new target for therapy". Vascular Medicine. 5 (1): 49–53. doi:10.1177/1358836X0000500108. ISSN 1358-863X. PMID 10737156.
  27. ^ Nazario B (September 17, 2021). "How Your Heart Works". WebMD.
  28. ^ Yeo J, Shahidi F (2021), "Bioactive peptides in health and disease: an overview", Biologically Active Peptides, Elsevier, pp. 1–26, doi:10.1016/b978-0-12-821389-6.00007-8, ISBN 978-0-12-821389-6, retrieved October 30, 2024
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  30. ^ "Factors that Affect Blood Pressure" (PDF). Archived from the original (PDF) on May 17, 2017. Retrieved October 21, 2018.
  31. ^ Nishida N, Yano H, Nishida T, et al. (September 2006). "Angiogenesis in cancer". Vascular Health and Risk Management. 2 (3): 213–219. doi:10.2147/vhrm.2006.2.3.213. PMC 1993983. PMID 17326328.
  32. ^ "World Heart Report 2023" (PDF). World Heart Federation. Geneva, Switzerland: 5. 2023.
  33. ^ CDC (October 24, 2024). "Heart Disease Facts". Heart Disease. Retrieved October 30, 2024.
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  35. ^ Gidaspow D (1994). Multiphase flow and fluidization : continuum and kinetic theory descriptions. Boston: Academic Press. ISBN 978-0-12-282470-8.
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