In our lab, two neurovascular mechanisms required for functional integrity of the skin are studied. The pressure-Induced vasodilation (PIV) is a protective mechanism, which delays the occurrence of tissue ischemia likely protecting the skin against pressure. Previous studies suggested the contribution of the central nervous system in this mechanism. In the first part of my PhD, we studied the spinal sensory transduction involvement in PIV and verify whether the lack of PIV increased incidence of pressure-induced ischemic lesions in healthy rats. We showed that spinal sensory disruption led to the loss of cutaneous PIV directly associated with increased incidence and severity of cutaneous lesions in response to prolonged ischemic compression in healthy animals. The current-induced vasodilation (CIV) is a neurovascular mechanism decribed as axon reflex mechanism. Exclusively studied in humans, the understanding of involved mechanisms remains limited. In the second part of my PhD, we aimed to develop an animal model and precise the underlying mechanisms involved in cathodal CIV. That we developed, we proved the involvement of the COX1/PGIS/PGI2/IP pathway, the cutaneous TRPV1 and ASIC channels present on capsaicin-sensitive fibres and the cutaneous CGRP and NK1 receptors in cathodal CIV in healthy rats. To conclude, PIV is an interesting tool to evaluate the protective capacities of the skin to withstand pressure in healthy conditions. CIV by reflecting the endogenous release of PGI2 in healthy skin offers a novel tool in complement to acetylcholine response in order to assess global capacities of the endothelium
