After blood flow has initially increased, there comes a period of increased vascular permeability resulting in exudation of plasma proteins and tissue oedema. The normal balance of capillary oncotic and hydrostatic pressure is disrupted.
For mild injury, released cytokines such as histamine and bradykinin act on venules to cause endothelial cell contraction, thus opening gaps between cells. On an ultrastructural level, these mediators initially cause a rise in inositol triphosphate and then intercellular released cytoplasmic calcium which peaks after 30 seconds. Later, extracellular calcium leaks into the cell over a prolonged period. Calcium causes the contraction of actin-myosin filaments. This leads to the opening of intercellular gaps between cells by up to 1 micrometre.
More severe injury may result in a simple mechanical breach of the endothelial wall. Other cytokines involved with increasing vascular pemeability include:
A late and extended leak of plasma may occur in certain circumstances e.g. thermal injuries such as sunburn, radiation exposure such as radiography, and in type IV hypersensitivity reactions.
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