 we have seen the interplay between proquagulants and anti-quagulants in some other videos. Similarly, the clot once formed, the duration for which it stayed is controlled by interplay between fibrin formation, factors causing fibrinolysis and inhibitors of fibrinolysis. So, these processes will ultimately lead to fibrin dissolution. So, it is important that fibrin once formed need to be removed also and finally tissue repair will take place. So, there are a number of proteins which are responsible for fibrinolysis and what they cause is break down fibrin to its degradation products. So, these degradation products are known as D-dimers. So, this is what about a protein known as plasmin. Now, plasmin itself is produced from plasminogen. Now, plasminogen is a protein which is produced in liver. So, normally this plasminogen is not converted to plasmin and only at the site of clot formation is this conversion taking place. So, this limits the activity of the plasmin to the site of clot formation. It is important because this plasmin also have the ability to break down fibrinogen and if it is active, it will break down fibrinogen all over the circulation. So, this plasminogen activation at the site of clot formation occurs by tissue plasminogen activators. Tissue, ticotissue plasminogen activators. These tissue plasminogen activators are released from endothelial cells of the vessels. It is interesting to know the thrombin which was crucial information of fibrin meshwork at the site of the vessel injury also needs to release of this TPA from the endothelial cells. So, at the site of vessel injury itself, this tissue plasminogen activator is released that is why plasmin is formed and which breaks down the fibrin meshwork to D-dimers. So, there is a whole system existing for localizing this activity to the site of vessel injury. Not only that, the activity of tissue plasminogen activator is most enhanced in the presence of fibrin. So, only when this tissue plasminogen activator and plasminogen bind with fibrin meshwork, it can lead to its breakdown. Next, any active plasmin at other places circulating in blood is inhibited by another protein known as alpha 2 plasmin. Now, this alpha 2 plasmin is also present at the site of a scler injury, but its activity becomes less once plasmin is bind with the fibrin. So, that inactivation of plasmin rate at the site of vessel injury is very less. At other sites, there is also inhibition of tissue plasminogen activator by plasminogen activator inhibitor released from endothelial cells. So, at normal places plasmin is kept in check by alpha 2 plasmin and tissue plasminogen activators are kept in check by plasminogen activator inhibitors. So, the system is such that all the process is localized at the site of the injury and also because of the factors which are leading to fibrin formation like thrombin, also activate factors which lead to its dissolution. So, there is a temporal relationship in built in clot formation and clot dissolution. Now, pharmacologically, this process of fibrinolysis is required when there is acute occlusion of arteries by thrombus or embolus. In that case, plasminogen activators are given intravenously to dissolve the thrombus formed in an unnecessary place.