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Hyperaemia or 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. Clinically, hyperaemia in tissues manifest as erythema, because of the engorgement of vessels with oxygenated blood. Hyperaemia can also occur due to a fall in atmospheric pressure outside the body.
Hyperaemia and the 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 activity there is a well-characterized fall in the partial pressure of oxygen and pH, 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.
When cells within the body are active in one way or another, they use more oxygen and fuel, such as glucose or fatty acids, than when they are not. Increased metabolic processes create more metabolic waste. The byproducts of metabolism are vasodilators. (Vasodilating metabolites: CO2, H+, K+, lactate, adenosine) Local arterioles respond to metabolism by dilatating, allowing more blood to reach the tissue. This prevents deprivation of the tissue. 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
Conversely, when a tissue is less metabolically active, it produces fewer metabolites which are simply washed away in blood flow.
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.
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:
- The brain through the neuron-dependent haemodynamic response.
- Penile erection tissue by release of nitric oxide.
Reactive hyperaemia or venous hyperemia is the transient increase in organ blood flow that occurs following a brief period of ischaemia. Following ischaemia there will be a shortage of oxygen and a build-up of metabolic waste.
This is commonly tested in the legs using Buerger's test.
Reactive hyperaemia often occurs as a consequence of Raynaud's phenomenon, where the vasospasm in the vasculature leads to ischaemia and necrosis of tissue and thus a subsequent increase in blood flow to remove the waste products and clear up cell debris.
- Jon Aster, Vinay Kumar, Abul K. Abbas; Nelson Fausto (2009). Robbins & Cotran Pathologic Basis of Disease (8th ed.). Philadelphia: Saunders. p. 113. ISBN 1-4160-3121-9.
- 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. PMID 26426256. Retrieved 13 September 2016.
- Active and reactive hyperemia. Richard E. Klabunde, Ph.D. Cardiovascular Physiology Concepts. Accessed on 27 February 2006.