Hyperaemia

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Hyperemia
Other namesHyperæmia, hyperemia

Hyperaemia (also hyperemia) is the increase of blood flow to different tissues in the body. It can have medical implications but is also a regulatory response, allowing change in blood supply to different tissues through vasodilation (widening of blood vessels). Clinically, hyperaemia in tissues manifests as erythema (redness of the skin) because of the engorgement of vessels with oxygenated blood. [1] Hyperaemia can also occur due to a fall in atmospheric pressure outside the body. The term comes from Greek ὑπέρ (hupér) 'over',andαἷμα (haîma) 'blood'.

Contents

Regulation of blood flow

Functional hyperaemia is an increase in blood flow to a tissue due to the presence of metabolites and a change in general conditions. When a tissue increases its activity, there is a well-characterized fall in the partial pressure of oxygen and pH, along with an increase in partial pressure of carbon dioxide, and a rise in temperature and the concentration of potassium ions. The mechanisms of vasodilation are predominantly local metabolites and myogenic effects. Increased metabolic activity of the tissue leads to a local increase in the extracellular concentration of such chemicals as adenosine, carbon dioxide, and lactic acid, and a decrease in oxygen and pH. These changes cause significant vasodilation. The reverse occurs when metabolic activity is slowed and these substances wash out of the tissues. The myogenic effect refers to the inherent attempt of vascular smooth muscle surrounding arterioles and arteries to maintain the tension in the wall of these blood vessels by dilating when internal pressure is reduced and to constrict when wall tension increases. [2]

Functional hyperaemia

Functional hyperaemia, metabolic hyperaemia, arterial hyperaemia or active hyperaemia, is the increased blood flow that occurs when tissue is active. [3]

Hyperaemia is likely mediated by the increased synthesis and/or release of vasodilatory agents during periods of heightened cellular metabolism. The increase in cellular metabolism causes the increase in vasoactive metabolic byproducts. Some of the putative vasodilatory agents (associated with metabolism) include, but are not limited to: carbon dioxide (CO2), hydrogen ion (H+), potassium (K+), adenosine (ADO), nitric oxide (NO)). These vasodilators released from the tissue act on local arterioles causing vasodilation, this causes a decrease in vascular resistance and allows an increase in blood flow to be directed toward the capillary bed of the active tissue. This increase allows the blood to serve the increased metabolic demand of the tissue and prevents a mismatch between O2-demand O2-supply. Recent research has suggested that the locally produced vasodilators may be acting in a redundant manner, in which the antagonism of one dilator, (be it pharmacologically or pathologically), may be compensated for by another in order to preserve blood flow to tissue. [4] While the locus of blood flow control (at least in skeletal muscle tissue) is widely thought to reside at the level of the arteriole, research has begun to suggest that capillary endothelial cells may be coordinators of skeletal muscle blood flow during functional hyperaemia. It is thought that vasodilators (released from active muscle fibers) can stimulate a local capillary endothelial cells which, in turn, causes the conduction of a vasodilatory signal to upstream arterioles, this then elicits arteriolar vasodilation consequently, creating a pathway of least resistance so blood flow can be precisely direct to capillaries supplying the metabolically active tissue. [5]

Conversely, when a tissue is less metabolically active, it produces fewer metabolites which are simply washed away in blood flow.[ citation needed ]

Since most of the common nutrients in the body are converted to carbon dioxide when they are metabolized, smooth muscle around blood vessels relax in response to increased concentrations of carbon dioxide within the blood and surrounding interstitial fluid. The relaxation of this smooth muscle results in vascular dilation and increased blood flow.[ citation needed ]

Some tissues require oxygen and fuel more quickly or in greater quantities. Examples of tissues and organs that are known to have specialized mechanisms for functional hyperaemia include:[ citation needed ]

Reactive hyperaemia

Reactive hyperemia, classified under arterial hyperemia, refers to the temporary increase in blood flow to an organ that follows a short period of ischemia or ischaemia. This condition arises due to a shortage of oxygen and an accumulation of metabolic waste resulting from the ischemic episode. A common method to assess this condition, particularly in the legs, is through Buerger's test. Furthermore, reactive hyperemia is frequently associated with Raynaud's phenomenon. In this scenario, vasospasm within the blood vessels leads to ischemia, which can cause tissue necrosis. Subsequently, there is an increased blood flow to the affected area, aimed at eliminating waste products and clearing cellular debris. [6]

Related Research Articles

<span class="mw-page-title-main">Blood vessel</span> Tubular structure of the circulatory system which transports blood

Blood vessels are the components of the circulatory system that transport blood throughout the human body. These vessels transport blood cells, nutrients, and oxygen to the tissues of the body. They also take waste and carbon dioxide away from the tissues. Blood vessels are needed to sustain life, because all of the body's tissues rely on their functionality.

<span class="mw-page-title-main">Capillary</span> Smallest type of blood vessel

A capillary is a small blood vessel, from 5 to 10 micrometres in diameter, and is part of the microcirculation system. Capillaries are microvessels and the smallest blood vessels in the body. They are composed of only the tunica intima, consisting of a thin wall of simple squamous endothelial cells. They are the site of the exchange of many substances from the surrounding interstitial fluid, and they convey blood from the smallest branches of the arteries (arterioles) to those of the veins (venules). Other substances which cross capillaries include water, oxygen, carbon dioxide, urea, glucose, uric acid, lactic acid and creatinine. Lymph capillaries connect with larger lymph vessels to drain lymphatic fluid collected in microcirculation.

<span class="mw-page-title-main">Angiogenesis</span> Blood vessel formation, when new vessels emerge from existing vessels

Angiogenesis is the physiological process through which new blood vessels form from pre-existing vessels, formed in the earlier stage of vasculogenesis. Angiogenesis continues the growth of the vasculature mainly by processes of sprouting and splitting, but processes such as coalescent angiogenesis, vessel elongation and vessel cooption also play a role. Vasculogenesis is the embryonic formation of endothelial cells from mesoderm cell precursors, and from neovascularization, although discussions are not always precise. The first vessels in the developing embryo form through vasculogenesis, after which angiogenesis is responsible for most, if not all, blood vessel growth during development and in disease.

<span class="mw-page-title-main">Smooth muscle</span> Involuntary non-striated muscle

Smooth muscle is an involuntary non-striated muscle, so-called because it has no sarcomeres and therefore no striations. It is divided into two subgroups, single-unit and multiunit smooth muscle. Within single-unit muscle, the whole bundle or sheet of smooth muscle cells contracts as a syncytium.

<span class="mw-page-title-main">Vasoconstriction</span> Narrowing of blood vessels due to the constriction of smooth muscle cells

Vasoconstriction is the narrowing of the blood vessels resulting from contraction of the muscular wall of the vessels, in particular the large arteries and small arterioles. The process is the opposite of vasodilation, the widening of blood vessels. The process is particularly important in controlling hemorrhage and reducing acute blood loss. When blood vessels constrict, the flow of blood is restricted or decreased, thus retaining body heat or increasing vascular resistance. This makes the skin turn paler because less blood reaches the surface, reducing the radiation of heat. On a larger level, vasoconstriction is one mechanism by which the body regulates and maintains mean arterial pressure.

<span class="mw-page-title-main">Microcirculation</span> Circulation of the blood in the smallest blood vessels

The microcirculation is the circulation of the blood in the smallest blood vessels, the microvessels of the microvasculature present within organ tissues. The microvessels include terminal arterioles, metarterioles, capillaries, and venules. Arterioles carry oxygenated blood to the capillaries, and blood flows out of the capillaries through venules into veins.

<span class="mw-page-title-main">Juxtaglomerular apparatus</span> Structure that regulates function of each nephron

The juxtaglomerular apparatus is a structure in the kidney that regulates the function of each nephron, the functional units of the kidney. The juxtaglomerular apparatus is named because it is next to (juxta-) the glomerulus.

<span class="mw-page-title-main">Vasodilation</span> Widening of blood vessels

Vasodilation, also known as vasorelaxation, is the widening of blood vessels. It results from relaxation of smooth muscle cells within the vessel walls, in particular in the large veins, large arteries, and smaller arterioles. The process is the opposite of vasoconstriction, which is the narrowing of blood vessels.

<span class="mw-page-title-main">Arteriole</span> Small arteries in the microcirculation

An arteriole is a small-diameter blood vessel in the microcirculation that extends and branches out from an artery and leads to capillaries.

Vascular resistance is the resistance that must be overcome to push blood through the circulatory system and create blood flow. The resistance offered by the systemic circulation is known as the systemic vascular resistance (SVR) or may sometimes be called by the older term total peripheral resistance (TPR), while the resistance offered by the pulmonary circulation is known as the pulmonary vascular resistance (PVR). Systemic vascular resistance is used in calculations of blood pressure, blood flow, and cardiac function. Vasoconstriction increases SVR, whereas vasodilation decreases SVR.

<span class="mw-page-title-main">Endothelial dysfunction</span>

In vascular diseases, endothelial dysfunction is a systemic pathological state of the endothelium. Along with acting as a semi-permeable membrane, the endothelium is responsible for maintaining vascular tone and regulating oxidative stress by releasing mediators, such as nitric oxide, prostacyclin and endothelin, and controlling local angiotensin-II activity.

<span class="mw-page-title-main">Haemodynamic response</span>

In haemodynamics, the body must respond to physical activities, external temperature, and other factors by homeostatically adjusting its blood flow to deliver nutrients such as oxygen and glucose to stressed tissues and allow them to function. Haemodynamic response (HR) allows the rapid delivery of blood to active neuronal tissues. The brain consumes large amounts of energy but does not have a reservoir of stored energy substrates. Since higher processes in the brain occur almost constantly, cerebral blood flow is essential for the maintenance of neurons, astrocytes, and other cells of the brain. This coupling between neuronal activity and blood flow is also referred to as neurovascular coupling.

Aerospace physiology is the study of the effects of high altitudes on the body, such as different pressures and levels of oxygen. At different altitudes the body may react in different ways, provoking more cardiac output, and producing more erythrocytes. These changes cause more energy waste in the body, causing muscle fatigue, but this varies depending on the level of the altitude.

In blood vessels Endothelium-Derived Hyperpolarizing Factor or EDHF is proposed to be a substance and/or electrical signal that is generated or synthesized in and released from the endothelium; its action is to hyperpolarize vascular smooth muscle cells, causing these cells to relax, thus allowing the blood vessel to expand in diameter.

In the physiology of the kidney, tubuloglomerular feedback (TGF) is a feedback system inside the kidneys. Within each nephron, information from the renal tubules is signaled to the glomerulus. Tubuloglomerular feedback is one of several mechanisms the kidney uses to regulate glomerular filtration rate (GFR). It involves the concept of purinergic signaling, in which an increased distal tubular sodium chloride concentration causes a basolateral release of adenosine from the macula densa cells. This initiates a cascade of events that ultimately brings GFR to an appropriate level.

The myogenic mechanism is how arteries and arterioles react to an increase or decrease of blood pressure to keep the blood flow constant within the blood vessel. Myogenic response refers to a contraction initiated by the myocyte itself instead of an outside occurrence or stimulus such as nerve innervation. Most often observed in smaller resistance arteries, this 'basal' myogenic tone may be useful in the regulation of organ blood flow and peripheral resistance, as it positions a vessel in a preconstricted state that allows other factors to induce additional constriction or dilation to increase or decrease blood flow.

Cerebral autoregulation is a process in mammals that aims to maintain adequate and stable cerebral blood flow. While most systems of the body show some degree of autoregulation, the brain is very sensitive to over- and underperfusion. Cerebral autoregulation plays an important role in maintaining an appropriate blood flow to that region. Brain perfusion is essential for life, since the brain has a high metabolic demand. By means of cerebral autoregulation, the body is able to deliver sufficient blood containing oxygen and nutrients to the brain tissue for this metabolic need, and remove CO2 and other waste products.

Microvasculature comprises the microvessels – venules and capillaries of the microcirculation, with a maximum average diameter of 0.3 millimeters. As the vessels decrease in size, they increase their surface-area-to-volume ratio. This allows surface properties to play a significant role in the function of the vessel.

In physiology, acute local blood flow regulation refers to an intrinsic regulation, or control, of the vascular tone of arteries at a local level, meaning within a certain tissue type, organ, or organ system. This intrinsic type of control means that the blood vessels can automatically adjust their own vascular tone, by dilating (widening) or constricting (narrowing), in response to some change in the environment. This change occurs in order to match up the tissue's oxygen demand with the actual oxygen supply available in the blood as closely as possible. For example, if a muscle is being utilized actively, it will require more oxygen than it was at rest, so the blood vessels supplying that muscle will vasodilate, or widen in size, to increase the amount of blood, and therefore oxygen, being delivered to that muscle.

A resistance artery is small diameter blood vessel in the microcirculation that contributes significantly to the creation of the resistance to flow and regulation of blood flow. Resistance arteries are usually small arteries or arterioles and include precapillary sphincters. Having thick muscular walls and narrow lumen they contribute the most to the resistance to blood flow. Degree of the contraction of vascular smooth muscle in the wall of a resistance artery is directly connected to the size of the lumen.

References

  1. ↑ Jon Aster; Vinay Kumar; Abul K. Abbas; Nelson Fausto (2009). Robbins & Cotran Pathologic Basis of Disease (8th ed.). Philadelphia: Saunders. p. 113. ISBN   978-1-4160-3121-5.
  2. ↑ Davis, Michael J.; Hill, Michael A. (1999-04-01). "Signaling Mechanisms Underlying the Vascular Myogenic Response". Physiological Reviews. American Physiological Society. 79 (2): 387–423. doi:10.1152/physrev.1999.79.2.387. ISSN   0031-9333.
  3. ↑ Clifford, Philip S. (2011). "Local control of blood flow". Advances in Physiology Education. American Physiological Society. 35 (1): 5–15. doi:10.1152/advan.00074.2010. ISSN   1043-4046.
  4. ↑ Lamb, Iain; Murrant, Coral (15 November 2015). "Potassium inhibits nitric oxide and adenosine arteriolar vasodilatation via KIR and Na+/K+ATPase: implications for redundancy in active hyperaemia". Journal of Physiology. 593 (23): 5111–5126. doi:10.1113/JP270613. PMC   4666990 . PMID   26426256.
  5. ↑ Murrant, Coral L.; Lamb, Iain R.; Novielli, Nicole M. (2016-12-30). "Capillary endothelial cells as coordinators of skeletal muscle blood flow during active hyperaemia". Microcirculation. 24 (3): e12348. doi:10.1111/micc.12348. ISSN   1549-8719. PMID   28036147. S2CID   3706150.
  6. ↑ "CV Physiology | Reactive Hyperemia". cvphysiology.com. Retrieved 2023-12-14.


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