Does the skin of mildly hyperthermic individuals display local variations in thermosensitivity for the control of skin blood flow?
© Burdon et al.; 2015
Published: 14 September 2015
In an accompanying communication, it was revealed that local variations in cutaneous thermosensitivity, with respect to the control of skin blood flow, were not evident in normothermic individuals. Previously, greater thermosensitivity of the face relative to other sites, including the hand and thigh, was observed for sudomotor control in mildly hyperthermic individuals. Therefore, the possibility was tested that such variations may also exist for vasomotor control when subjects were first rendered mildly hyperthermic.
Seven subjects (4 females and 3 males) participated in two trials. Hand and forearm blood flows (right side) were measured in separate trials (water-displacement plethysmography). Deep-body (aural) and skin temperatures were elevated and clamped (whole-body, water-perfusion suit), and then three skin sites (face, hand, thigh; left side) were thermally stimulated (water-perfusion patches). Local skin temperatures were elevated and reduced ~5°C from baseline. Vasomotor sensitivity was calculated for each stimulation from the change in segmental blood flow divided by the change in skin temperature at each treated site.
Vasomotor sensitivity of the hand and forearm (combined) during three local thermal stimuli.
Hand and forearm vasomotor sensitivity (mL.100 mL tissue-1.°C-1.min-1)
1.04 (SD 0.55)*
0.64 (SD 0.50)*
1.28 (SD 0.82)*
0.63 (SD 0.42)*
0.59 (SD 0.29)
0.50 (SD 0.43)
Consistent with previous sudomotor research, the face, and now also the hand, displayed greater cutaneous thermosensitivity in mildly hyperthermic subjects. These vascular responses are consistent with the representation of each treated site within the sensory cortex (homunculus), and this may also relate to local variations in thermoreceptor density. The fact that this pattern was not apparent within normothermic individuals (accompanying communication) can be explained by the fact that, in that state, vasomotor drive is dominated by the thermal status of the deep-body tissues. Thus, the centrally mediated vasoconstrictor tone was neither over-ridden nor enhanced by these localised thermal stimuli.
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