What happens to small blood vessels immediately after tissue injury?

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Pathways of complement activation — inflammation The main function of complement proteins is to aid in the destruction of pathogens by piercing their outer membranes (cell lysis) or by making them more attractive to phagocytic cells such as macrophages (a process known as opsonization). Some complement components also promote inflammation by stimulating cells to release histamine and by attracting phagocytic cells to the site of infection.

Immediately following tissue injury, the small blood vessels in the affected area undergo a momentary constriction known as vasoconstriction.12

While this initial contraction is transient and considered of little significance to the broader inflammatory response, it serves as a primary hemostatic mechanism to minimize blood loss. Following this brief period, the blood vessels undergo vasodilation, which increases blood flow to the site of injury. Subsequently, the vessel walls become more permeable, allowing protein-rich fluid, known as exudate, to enter the surrounding tissues. This shift in vascular dynamics causes blood flow to become more sluggish, facilitating the movement of white blood cells toward the vessel walls so they can eventually emigrate into the tissue.12