Non-freezing
cold injury is a prevalent cause of peripheral nerve damage, but its pathogenic mechanism is poorly understood, and treatment remains inadequate.
Glucocorticoids have anti-inflammatory and lipid peroxidation-inhibiting properties. We therefore examined whether
dexamethasone, a synthetic
glucocorticoid compound, would alleviate early-stage non-freezing
cold injury of the sciatic nerve. We established Wistar rat models of non-freezing
cold injury by exposing the left sciatic nerve to cold (3-5°C) for 2 hours, then administered
dexamethasone (3 mg/kg intraperitoneally) to half of the models. One day after injury, the concentration of
Evans blue tracer in the injured sciatic nerve of rats that received
dexamethasone was notably lower than that in the injured sciatic nerve of rats that did not receive
dexamethasone; neither
Evans blue dye nor capillary
stenosis was observed in the endoneurium, but myelinated nerve fibers were markedly degenerated in the injured sciatic nerve of animals that received
dexamethasone. After
dexamethasone administration, however, endoneurial vasculopathy was markedly improved, although damage to the myelinated nerve fiber was not alleviated. These findings suggest that
dexamethasone protects the blood-nerve barrier, but its benefit in non-freezing
cold injury is limited to the vascular system.