Vascular Injury, Effects, Blood Clot Formation

• Vascular surgery creates vascular injury at the anastomosis.
• Upon vascular injury:
  • The endothelial cell lining of the vessel lumen is disrupted and the underlying smooth muscle and collagen fibers are exposed to the circulation.
  • Von Willebrand Factor binds to exposed collagen fibers through its A3 domain.
  • Collagen-bound von Willebrand Factor then binds to platelets through the GP Ibα receptor.
  • This interaction acts to tether platelets to thrombogenic surfaces even during rapid blood flow.
  • Shear forces from blood flow propel the tethered platelet forward where it comes in contact with exposed collagen.
  • The platelet then binds collagen through integrin receptors, and platelet activation occurs.
  • Activated platelets release a variety of factors that attract and activate additional platelets at the site of injury to amplify platelet aggregation.
  • Additional clotting mechanisms result in the production of fibrin which forms dense interlocking strands which help to secure the clot.
  • Over time, the factors released by activated platelets also attract vascular smooth muscle cells from the media and adventitia to migrate to the intima of the vessel wall.
  • As these smooth muscle cells migrate and proliferate they cause thickening of the vessel wall and narrowing of the lumen.
  • This narrowing restricts blood flow and may eventually lead to thrombosis and complete occlusion of the blood vessel.