Abstract
Skin is constantly subjected to pressure at different levels. Pressure-induced vasodilation (PIV) is one of the response mechanisms to low pressure that maintains the homeostasis of the skin. PIV results from the interaction of primary afferent nerves and vascular endothelium of skin vessels. Thanks to this cutaneous neuro-vascular interaction, the cutaneous blood flow increase allows the maintenance of an optimal level of oxygenation and minimizes the lack of vascularization of the skin tissue under low pressure. It seems to be associated with the cutaneous protection mechanisms to prevent pressure ulcers. In some contexts, where microangiopathy and neuropathy can occur, such as aging and diabetes, PIV is impaired, leading to a dramatic early decrease in local skin blood flow when low pressure is applied. In aging, PIV alteration is due to endothelial dysfunction, essentially from an alteration of the nitric oxide pathway. In the inflamm-aging context, oxidative stress increases leading to endothelial cell and nerve damages. An age-related sensory neuropathy will exacerbate the alteration of PIV during the aging process. In diabetes, non-controlled hyperglycaemia leads to an increase in several pathological biochemical pathways that involve oxidative stress and can affect PIV. Sorbinil, alagebrium and alpha-lipoic acid are able individually to restore PIV through a possible oxidative stress reduction. Candesartan, an angiotensin II type 1 receptor blocker, is also able to restore PIV and prevent pressure ulcer formation. The possibility of preventing pressure ulcer associated to diabetes and/or aging with the restoration of PIV seems to be a promising research path.
Highlights
Only potassium channels have been studied in the relaxation mechanism of pressure-induced vasodilation (PIV), but calcium channels might be involved, as in other muscle cells (Zamponi et al, 2015). This cascade of events causes vasodilation, allowing skin blood flow to increase from baseline, which delays the decrease in cutaneous blood flow produced by local application of low pressure to the healthy skin, a physiologically appropriate adjustment of local vasomotor function (Figure 2)
Margolis et al (2010) carried out a retrospective study in the United Kingdom on 40,342 diabetic patients in 2010. They looked at the differential effect of angiotensin II type receptor blocker (ARB) and angiotensin-converting enzyme inhibitors (ACEi), notably on diabetic foot ulcer (DFU)
Pressure-induced vasodilation is an important mechanism of cutaneous homeostasis in response to low pressure
Summary
The skin, nervous system and immune system are not independent systems but are closely associated and use the same language of cytokines and neurotransmitters in the context of the neuroimmunocutaneous system (Misery, 1997). It allows an increase in the skin blood flow and helps keep an optimal level of oxygenation in the skin even with pressure on it This mechanism of response to low pressure, called pressure-induced vasodilation (PIV), was first described in humans (Fromy et al, 1998). Only potassium channels have been studied in the relaxation mechanism of PIV, but calcium channels might be involved, as in other muscle cells (Zamponi et al, 2015) This cascade of events causes vasodilation, allowing skin blood flow to increase from baseline, which delays the decrease in cutaneous blood flow produced by local application of low pressure to the healthy skin, a physiologically appropriate adjustment of local vasomotor function (Figure 2)
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