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.
Study Type
INTERVENTIONAL
Allocation
NON_RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
QUADRUPLE
Enrollment
20
diclofenac 5% vs placebo (topical application) cutaneous blood flow measurement using laser Doppler
amiloride 1mM vs placebo (intradermal injection) cutaneous blood flow measurement using laser Doppler
Pôle d'activité medicale-Centre Hospitalier Lyon Sud-Hospices Civils de Lyon
Pierre-Bénite, France
evaluate the difference in the cutaneous microvascular response to local pressure application between treated (amiloride and diclofenac) and untreated skin.
Time frame: Criteria will be measured 30 and 60 minutes following the injection of amiloride and the application of diclofenac, respectively.
Evaluate difference in the cutaneous sensitivity and the cutaneous microvascular response to acetylcholine, sodium nitroprusside, electrical current and local heating between treated (amiloride and diclofenac) and untreated skin
Time frame: Criteria will be measured 30 and 60 minutes following the injection of amiloride and the application of diclofenac, respectively.
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