Pressure ulcers are a common and costly problem. Advancing the understanding regarding the
basic pathophysiological mechanisms mediating the development of pressure ulcers will allow
for better delineation of populations at risk.
Healthy skin is protected from pressure-induced ischemic damage because of the presence of
pressure-induced vasodilation (PIV). In contrast, in absence of PIV, such as in diabetic
patients or older subjects with sensory neuropathy, the skin is exposed to severe cutaneous
ischemia, which could lead to pressure ulcer formation.
Since Acid Sensing Ion channels (ASICs) appear to be involved in the cutaneous
mechanosensitivity, the investigators hypothesized that PIV could be altered by treatments
that block ASICs.