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Prostaglandins are produced in the early stages of a burn injury. Key mediators include:
- prostaglandin E2; it increases vascular permeability
- leukotrienes B4 to D4 increase vascular permeability
- prostaglandin I2; vasodilator and increased vascular permeability
- thromboxane A2; causes vasoconstriction in the zone around the burn, so extending the zone of necrosis
- platelets - for thromboxane A2
In a sheep burn model, anti-inflammatory drugs reduce the levels of prostaglandins but have little effect on oedema.
Last reviewed 01/2018