Increased vascular permeability evoked by cold injury

The inflammatory response induced by mild freezing of the skin of the rat is monophasic and short-lived. Increments in the intensity and/or duration of the stimulus increase the magnitude of the initial exudation, as well as evoking a biphasic response. Nevertheless, the initial response always dominates the permeability effects. Relatively severe freezing provokes marked and prolonged exudation. The permeability response involves both venules and capillaries in all its phases, although the initial leakage is predominantly from venules. Progressive increase in the severity of the stimulus enhances capillary labelling and, as judged histologically, causes considerable vascular damage. Histological damage is reversible with freezing severe enough to elicit a delayed permeability response, but stronger stimulation results in compaction stasis, endothelial damage and necrosis of skin.