22.23:
Clot Retraction and Fibrinolysis
The activated platelets in a blood clot extend projections and interact with other platelets and fibrin fibers.
Within 30 to 60 minutes, the contractile proteins in these platelet projections start pulling the fibrin strands to initiate clot retraction.
As a result, the clot reduces in size, bringing the edges of the damaged vessel closer together.
Simultaneously, platelets primarily release two growth factors to stimulate different cell types for injury repair.
Platelet-derived growth factor promotes cell division and growth of the smooth muscle and fibroblasts from the surrounding connective tissue to rebuild the vessel wall.
On the other hand, the vascular endothelial growth factor restores the endothelial lining of the blood vessel.
As the injury heals, the neighboring endothelial cells secrete tissue plasminogen activator, which activates a plasma protein called plasminogen trapped within the fibrin mesh.
The activated plasminogen, called plasmin, breaks down the clot by digesting fibrin threads. This process, called fibrinolysis, starts within two days of clot retraction and clears the vessel.
22.23:
Clot Retraction and Fibrinolysis
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Simultaneously, growth factors released from platelets begin their work to heal the injury permanently. Two key factors in this process are platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF). PDGF stimulates cell division and growth, encouraging the regeneration of damaged tissues. On the contrary, VEGF aids the formation of new blood vessels, known as angiogenesis. Together, these growth factors expedite the healing process, restoring the integrity of the damaged vessel.
Small clots develop when a minor injury or a developing atherosclerotic plaque occurs. However, the body's homeostatic mechanisms play a crucial role in regulating the size and formation of blood clots. When improper clots form, the fibrinolytic system plays a vital role in dissolving them. Plasminogen, a plasma protein, is incorporated into the clot during its formation. Plasmin is formed through the release of tissue plasminogen activator from endothelial cells and the activation of plasminogen by factors such as thrombin and factor XII. The active plasmin enzyme can break down fibrin threads and deactivate clotting substances.
Despite the positive feedback effect of thrombin, clot formation usually remains localized at the site of damage due to factors like fibrin absorption and the dispersal of clotting factors in the blood.
Moreover, endothelial cells and white blood cells produce prostacyclin, which regulates platelet adhesion and release. Anticoagulants like antithrombin and heparin also help regulate clotting by blocking specific factors and enhancing the effectiveness of plasminogen activators. These intricate mechanisms maintain a delicate balance, preventing excessive clotting while ensuring the formation of clots at the appropriate sites.