Blushing or erubescence is the reddening of a person's face due to psychological reasons. [1] [2] [3] It is normally involuntary and triggered by emotional stress associated with passion, embarrassment, shyness, fear, anger, or romantic stimulation.
Severe blushing is also common in people who have social anxiety in which the person experiences extreme and persistent anxiety in social and performance situations.
Blushing is generally distinguished, despite a close physiological relation, from flushing, which is more intensive and extends over more of the body, and seldom has a mental source. Idiopathic craniofacial erythema is a medical condition where a person blushes strongly with little or no provocation. People who have social phobia are particularly prone to idiopathic craniofacial erythema.
This needed needs additional citations for verification .(May 2024) |
A blush is a reddening of the cheeks and forehead brought about by increased capillary blood flow in the skin. It can also extend to the ears, neck and upper chest, an area termed the 'blush region'. [4]
There is evidence that the blushing region is anatomically different in structure. The facial skin, for example, has more capillary loops per unit area and generally more vessels per unit volume than other skin areas. In addition, blood vessels of the cheek are wider in diameter, are nearer the surface, and visibility is less diminished by tissue fluid. These specific characteristics of the architecture of the facial vessels led Wilkin in an overview of possible causes of facial flushing to the following conclusion: "[...] Increased capacity and greater visibility can account for the limited distribution of flushing". [5]
Evidence for special vasodilation mechanisms was reported by Mellander and his colleagues (Mellander, Andersson, Afzelius, & Hellstrand. 1982). They studied buccal segments of the human facial veins in vitro. Unlike veins from other areas of the skin, facial veins responded with an active myogenic contraction to passive stretch and were therefore able to develop an intrinsic basal tone. Additionally Mellander et al. showed that the veins in this specific area were also supplied with beta-adrenoceptors in addition to the common alpha-adrenoceptors. These beta-adrenoceptors could exert a dilator mechanism on the above-described basal tone of the facial cutaneous venous plexus. Mellander and his colleagues propose that this mechanism is involved in emotional blushing.
Drummond has partially confirmed this effect by pharmacological blocking experiments (Drummond. 1997). In a number of trials, he blocked both alpha-adrenergic receptors (with phentolamine) and beta-adrenergic receptors (with propranolol introduced transcutaneously by iontophoresis). Blushing was measured at the forehead using a dual channel laser Doppler flowmeter. Subjects were undergraduate students divided into frequent and infrequent blushers according to self-report. Their mean age was 22.9 years, which is especially favorable for assessing blushing, since young subjects are more likely to blush and blush more intensively. The subjects underwent several procedures, one of which was designed to produce blushing.
Alpha-adrenergic blockade with phentolamine had no influence on the amount of blushing in frequent or in infrequent blushers, indicating that release of sympathetic vasoconstrictor tone does not substantially influence blushing. This result was expected since vasoconstrictor tone in the facial area is known to be generally low (van der Meer. 1985). Beta-adrenergic blockade with propranolol on the other hand decreased blushing in both frequent and infrequent blushers. However, despite complete blockade, blood flow still increased substantially during the embarrassment and blushing inducing procedure. Additional vasodilator mechanisms must therefore be involved.
Charles Darwin devoted Chapter 13 of his 1872 The Expression of the Emotions in Man and Animals to complex emotional states including self-attention, shame, shyness, modesty and blushing. He described blushing as "... the most peculiar and most human of all expressions."
Several different psychological and psycho-physiological mechanisms for blushing have been hypothesized by Crozier (2010): "An explanation that emphasizes the blush's visibility proposes that when we feel shame we communicate our emotion to others and in doing so we send an important signal to them. It tells them something about us. It shows that we are ashamed or embarrassed, that we recognise that something is out of place. It shows that we are sorry about this. It shows that we want to put things right. To blush at innuendo is to show awareness of its implications and to display modesty that conveys that you are not brazen or shameless. The blush makes a particularly effective signal because it is involuntary and uncontrollable. Of course, a blush can be unwanted [but the] costs to the blusher on specific occasions are outweighed by the long-term benefits of being seen as adhering to the group and by the general advantages the blush provides: indeed the costs may enhance the signal's perceived value." [6] A number of techniques may be used to help prevent or reduce blushing. [7]
Salzen (2010) suggested that blushing and flushing were manifestations of the physiological impact of the instinctual fight/flight mechanism, when neither confrontation nor retreat is possible. [8]
Blushing has been linked to activation in the cerebellum and the left paracentral lobe. [9]
Beta blockers, also spelled β-blockers, are a class of medications that are predominantly used to manage abnormal heart rhythms (arrhythmia), and to protect the heart from a second heart attack after a first heart attack. They are also widely used to treat high blood pressure, although they are no longer the first choice for initial treatment of most patients.
Propranolol is a medication of the beta blocker class. It is used to treat high blood pressure, a number of types of irregular heart rate, thyrotoxicosis, capillary hemangiomas, performance anxiety, and essential tremors, as well to prevent migraine headaches, and to prevent further heart problems in those with angina or previous heart attacks. It can be taken orally or by intravenous injection. The formulation that is taken orally comes in short-acting and long-acting versions. Propranolol appears in the blood after 30 minutes and has a maximum effect between 60 and 90 minutes when taken orally.
The adrenergic receptors or adrenoceptors are a class of G protein-coupled receptors that are targets of many catecholamines like norepinephrine (noradrenaline) and epinephrine (adrenaline) produced by the body, but also many medications like beta blockers, beta-2 (β2) agonists and alpha-2 (α2) agonists, which are used to treat high blood pressure and asthma, for example.
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.
Flushing is to become markedly red in the face and often other areas of the skin, from various physiological conditions. Flushing is generally distinguished from blushing, since blushing is psychosomatic, milder, generally restricted to the face, cheeks or ears, and generally assumed to reflect emotional stress, such as embarrassment, anger, or romantic stimulation. Flushing is also a cardinal symptom of carcinoid syndrome—the syndrome that results from hormones being secreted into systemic circulation.
Atenolol is a beta blocker medication primarily used to treat high blood pressure and heart-associated chest pain. Although used to treat high blood pressure, it does not seem to improve mortality in those with the condition. Other uses include the prevention of migraines and treatment of certain irregular heart beats. It is taken orally or by intravenous injection. It can also be used with other blood pressure medications.
Rosacea is a long-term skin condition that typically affects the face. It results in redness, pimples, swelling, and small and superficial dilated blood vessels. Often, the nose, cheeks, forehead, and chin are most involved. A red, enlarged nose may occur in severe disease, a condition known as rhinophyma.
Vascular smooth muscle is the type of smooth muscle that makes up most of the walls of blood vessels.
Phenylephrine, sold under the brand names Neosynephrine and Sudafed PE among numerous others, is a medication used as a decongestant for uncomplicated nasal congestion, used to dilate the pupil, used to increase blood pressure, and used to relieve hemorrhoids. It can be taken by mouth, as a nasal spray, given by injection into a vein or muscle, applied to the skin, or as a rectal suppository.
Oxymetazoline, sold under the brand name Afrin among others, is a topical decongestant and vasoconstrictor medication. It is available over-the-counter as a nasal spray to treat nasal congestion and nosebleeds, as eye drops to treat eye redness due to minor irritation, and as a prescription topical cream to treat persistent facial redness due to rosacea in adults. Its effects begin within minutes and last for up to six hours. Intranasal use for longer than three to five days may cause congestion to recur or worsen, resulting in physical dependence.
Isoprenaline, also known as isoproterenol and sold under the brand name Isuprel among others, is a sympathomimetic medication which is used in the treatment of acute bradycardia, heart block, and rarely for asthma, among other indications. It is used by injection into a vein, muscle, fat, or the heart, by inhalation, and in the past under the tongue or into the rectum.
Labetalol is a medication used to treat high blood pressure and in long term management of angina. This includes essential hypertension, hypertensive emergencies, and hypertension of pregnancy. In essential hypertension it is generally less preferred than a number of other blood pressure medications. It can be given by mouth or by injection into a vein.
The alpha-2 (α2) adrenergic receptor is a G protein-coupled receptor (GPCR) associated with the Gi heterotrimeric G-protein. It consists of three highly homologous subtypes, including α2A-, α2B-, and α2C-adrenergic. Some species other than humans express a fourth α2D-adrenergic receptor as well. Catecholamines like norepinephrine (noradrenaline) and epinephrine (adrenaline) signal through the α2-adrenergic receptor in the central and peripheral nervous systems.
An adrenergic antagonist is a drug that inhibits the function of adrenergic receptors. There are five adrenergic receptors, which are divided into two groups. The first group of receptors are the beta (β) adrenergic receptors. There are β1, β2, and β3 receptors. The second group contains the alpha (α) adrenoreceptors. There are only α1 and α2 receptors. Adrenergic receptors are located near the heart, kidneys, lungs, and gastrointestinal tract. There are also α-adreno receptors that are located on vascular smooth muscle.
Adrenaline, also known as epinephrine, is a hormone and medication which is involved in regulating visceral functions. It appears as a white microcrystalline granule. Adrenaline is normally produced by the adrenal glands and by a small number of neurons in the medulla oblongata. It plays an essential role in the fight-or-flight response by increasing blood flow to muscles, heart output by acting on the SA node, pupil dilation response, and blood sugar level. It does this by binding to alpha and beta receptors. It is found in many animals, including humans, and some single-celled organisms. It has also been isolated from the plant Scoparia dulcis found in Northern Vietnam.
Alpha blockers, also known as α-blockers or α-adrenoreceptor antagonists, are a class of pharmacological agents that act as antagonists on α-adrenergic receptors (α-adrenoceptors).
Cocaine intoxication refers to the subjective, desired and adverse effects of cocaine on the mind and behavior of users. Both self-induced and involuntary cocaine intoxication have medical and legal implications.
The catecholamines are a group of neurotransmitters composed of the endogenous substances dopamine, noradrenaline (norepinephrine), and adrenaline (epinephrine), as well as numerous artificially synthesized compounds such as isoprenaline - an anti-bradycardiac medication. Their investigation constitutes a major chapter in the history of physiology, biochemistry, and pharmacology. Adrenaline was the first hormone extracted from an endocrine gland and obtained in pure form, before the word hormone was coined. Adrenaline was also the first hormone whose structure and biosynthesis was discovered. Second to acetylcholine, adrenaline and noradrenaline were some of the first neurotransmitters discovered, and the first intercellular biochemical signals to be found in intracellular vesicles. The β-adrenoceptor gene was the first G protein-coupled receptor to be cloned.
Serafim Guimarães, full name Serafim Correia Pinto Guimarães, is a Portuguese physician and pharmacologist. With his colleague Walter Osswald he made the Department of Pharmacology, Medical Faculty of the University of Porto, a center of research on catecholamines and the sympathetic nervous system, especially their relation to blood vessels.
Adrenergic blocking agents are a class of drugs that exhibit its pharmacological action through inhibiting the action of the sympathetic nervous system in the body. The sympathetic nervous system(SNS) is an autonomic nervous system that we cannot control by will. It triggers a series of responses after the body releases chemicals named noradrenaline and epinephrine. These chemicals will act on adrenergic receptors, with subtypes Alpha-1, Alpha-2, Beta-1, Beta-2, Beta-3, which ultimately allow the body to trigger a "fight-or-flight" response to handle external stress. These responses include vessel constriction in general vessels whereas there is vasodilation in vessels that supply skeletal muscles or in coronary vessels. Additionally, the heart rate and contractile force increase when SNS is activated, which may be harmful to cardiac function as it increases metabolic demand.