Editing Blushing (section)

==Physiology==
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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'.<ref>{{Cite web|url=https://thepsychologist.bps.org.uk/volume-23/edition-5/puzzle-blushing|title=The puzzle of blushing|website=thepsychologist.bps.org.uk|access-date=2019-05-25}}</ref>

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".<ref>''Journal of the American Academy of Dermatology'', Wilkin. 1988</ref>

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, therefore, were able to develop an intrinsic basal tone. Additionally Mellander et al. showed that the veins in this specific area were also supplied with beta-[[adrenoceptor]]s 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 receptor]]s (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 did not influence the amount of blushing in frequent or infrequent blushers, indicating that the 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.