Mechanism of Increased Vascular Permeability in Acute Inflammation

Several mechanisms involved in increased vascular permeability in acute inflammation:

1. Contraction of endothelial cells resulting in increased interendothelial spaces is the most common mechanism of vascular leakage.
2. Endothelial injury, resulting in endothelial cell necrosis and detachment.
3. Increased transport of fluids and proteins, called transcytosis, through the endothelial cell. This process may involve intracellular channels that may be stimulated by certain factors, such as vascular endothelial growth factor (VEGF), that promote vascular leakage.

What vascular changes occur in acute inflammation?

Vascular changes in acute inflammation are as follows:

1. Vasodilation is induced by the action of several mediators, mainly histamine, on vascular smooth muscle.
2. Vasodilation is quickly followed by increased permeability of the microvasculature.
3. Engorgement of small vessels with slowly moving red cells, a condition termed stasis,
   which is seen as vascular congestion and localized redness of the involved tissue.
4. As stasis develops, blood leukocytes, principally neutrophils, accumulate along the vascular endothelium.