Fouchard Maxime, Misery Laurent, Le Garrec Raphaële, Sigaudo-Roussel Dominique, Fromy Bérengère
LIEN, F-29200, University of Brest, Brest, France.
Department of Dermatology, University Hospital of Brest, Brest, France.
Front Physiol. 2019 Jul 3;10:862. doi: 10.3389/fphys.2019.00862. eCollection 2019.
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.
皮肤不断受到不同程度的压力。压力诱导的血管舒张（PIV）是皮肤对低压的一种反应机制，可维持皮肤的稳态。PIV是由皮肤血管的初级传入神经与血管内皮相互作用产生的。由于这种皮肤神经血管相互作用，皮肤血流增加有助于维持最佳的氧合水平，并最大限度地减少低压下皮肤组织血管化不足的情况。它似乎与预防压疮的皮肤保护机制有关。在某些可能发生微血管病变和神经病变的情况下，如衰老和糖尿病，PIV会受损，导致在施加低压时局部皮肤血流急剧早期减少。在衰老过程中，PIV改变是由于内皮功能障碍，主要是一氧化氮途径的改变。在炎症衰老的背景下，氧化应激增加导致内皮细胞和神经损伤。与年龄相关的感觉神经病变会在衰老过程中加剧PIV的改变。在糖尿病中，未控制的高血糖会导致涉及氧化应激的多种病理生化途径增加，并可能影响PIV。索比尼尔、阿拉吉瑞姆和α-硫辛酸能够分别通过可能降低氧化应激来恢复PIV。坎地沙坦是一种血管紧张素II 1型受体阻滞剂，也能够恢复PIV并预防压疮形成。通过恢复PIV来预防与糖尿病和/或衰老相关的压疮的可能性似乎是一条有前景的研究途径。
