Capillary permeability during acute inflammation

Capillary permeability during acute inflammation refers to the **transient increase in the ability of small blood vessels**—especially postcapillary venules—to allow fluids, proteins, and sometimes cells to pass from the bloodstream into surrounding tissues. This phenomenon is **regulated by chemical mediators** released at sites of injury or infection. During the vascular phase of acute inflammation, **endothelial cells contract**, widening intercellular gaps and increasing vascular barrier leakiness. The resulting exudation leads to local tissue swelling (**edema**) due to protein-rich fluid accumulation. This increased tissue fluid helps deliver immune proteins like complement and immunoglobulins while facilitating leukocyte migration into affected areas for pathogen clearance[3][4][7]. While often considered an inevitable part of inflammatory responses, recent research shows that **leukocyte emigration can occur independently from vascular leakage**, suggesting that targeting excessive capillary leak could be therapeutically beneficial without impairing host defense mechanisms[5]. Note: "Capillary permeability during acute inflammation" describes a physiological process rather than a discrete molecular entity or therapeutic target such as an enzyme or receptor. Therefore, it does not fit standard drug-target classification schemes[3][4]

Other names

Increased capillary permeability in inflammationVascular leakage during acute inflammationMicrovascular permeability in inflammation

Not applicable to a specific molecule; various mediators—such as histamine, bradykinin, and cytokines—increase capillary permeability via endothelial cell contraction and junctional changes[3][7]