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[Cutaneous vasodilation induced by local pressure application: modifications in diabetes]
1UMR CNRS 6188, Circulations Régionales et Micro Circulation, Faculté de médecine, 49045 Angers. jeanlouis.saumet@univ-angers.fr
Bulletin De L'Academie Nationale De Medecine
|August 27, 2005
Summary
Altered pressure-induced vasodilation, involving specific nerve fibers and nitric oxide, is linked to pressure sore risk. This mechanism is impaired in diabetes, suggesting therapeutic targets for prevention.
Area of Science:
- Physiology
- Dermatology
- Neurology
Context:
- Prolonged external pressure can lead to pressure sores.
- Mechanical sensitivity and cutaneous vasodilation are key factors.
- Patients at high risk for pressure sores may have altered vasodilation.
Purpose:
- To examine the link between mechanical sensitivity and cutaneous vasodilation.
- To investigate how this link is altered in patients at high risk of pressure sores.
- To explore the role of specific nerve fibers and molecules in pressure-induced vasodilation.
Summary:
- The link between mechanical sensitivity and cutaneous vasodilation is independent of inflammation or pain.
- Capsaicin-sensitive nerve fibers, receptors for calcitonin gene-related peptide, vasoactive intestinal peptide, and pituitary adenylate cyclase-activating polypeptide are involved.
- Endothelial nitric oxide is crucial for pressure-induced vasodilation, and this mechanism is altered in diabetes, even before neurological complications arise.
Impact:
- Understanding this link may help prevent pressure sores and plantar ulcers in diabetic patients.
- Restoring pressure-induced vasodilation could be a therapeutic strategy.
- Identifies potential molecular targets for preventing pressure-related tissue damage.