PHYSIOLOGY OF WOUND HEALING : Lotensin
Posted by Surgery on Jul 11, 2008
HEMOSTASIS
Formation of the Hemostatic Plug
Disruption of the normal tissue architecture with transection of blood vessels following injury, results in the exposure of blood elements to subendothelial collagen. This initiates coagulation by surface activation of Hageman factor, the release of tissue procoagulants from damaged cells and the exposure of phospholipids on activated platelets and endothelial cells (1: Lotensin ).
fibrinfibroblast
The key element that initiates the cascade is the surface absorption of coagulation proenzyme, which protects it from protease inhibitors and allows rapid amplification of the coagulation cascade leading to clot formation. The extent of clot formation is also regulated at the microvascular level by several factors, including production of prostacyclin, which inhibits platelet aggregation (2: Lotensin); antithrombin III, which inhibits the activity of thrombin (3: Lotensin ); protein C, which degrades coagulation factors V and VIII (4); and the release of plasminogen activator, which converts plasminogen to plasmin and initiates clot lysis (5). Plasminogen activator and plasmin are capable of degrading a large number of extracellular matrix proteins. Their activity is confined to cell surface microenvironment by the presence of plasminogen inhibitor bound to extracellular matrix protein (6).
Formation of the Hemostatic Plug : Pravachol
Posted by Surgery on Jul 11, 2008
Disruption of the normal tissue architecture with transection of blood vessels following injury, results in the exposure of blood elements to subendothelial collagen. This initiates coagulation by surface activation of Hageman factor, the release of tissue procoagulants from damaged cells and the exposure of phospholipids on activated platelets and endothelial cells (1: Pravachol ). The key element that initiates the cascade is the surface absorption of coagulation proenzyme, which protects it from protease inhibitors and allows rapid amplification of the coagulation cascade leading to clot formation.
fibrin
The extent of clot formation is also regulated at the microvascular level by several factors, including production of prostacyclin, which inhibits platelet aggregation (2: Pravachol); antithrombin III, which inhibits the activity of thrombin (3); protein C, which degrades coagulation factors V and VIII (4); and the release of plasminogen activator, which converts plasminogen to plasmin and initiates clot lysis (5). Plasminogen activator and plasmin are capable of degrading a large number of extracellular matrix proteins. Their activity is confined to cell surface microenvironment by the presence of plasminogen inhibitor bound to extracellular matrix protein (6: Pravachol ).
Once hemostasis has been established, a second major function of this primary hemostatic plug is to act as a provisional matrix, or a scaffold, for the recruitment of cells to the site of injury. Fibrin is a 340-kd hexamer composed of three fibrinogen chains that are coded on three different genes.
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