loading...| Preferred Name |
Hemostasis |
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| Synonyms |
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| Definitions |
Reviewed: Brummel, K, Rush, MG, Stafford, DW, 0000-00-00 00:00:00 Authored: D'Eustachio, P, Pace, N.P., Farndale, R, de Bono, B, 2004-01-21 22:18:59 Hemostasis is a physiological response that culminates in the arrest of bleeding from an injured vessel. Under normal conditions the vascular endothelium supports vasodilation, inhibits platelet adhesion and activation, suppresses coagulation, enhances fibrin cleavage and is anti-inflammatory in character. Under acute vascular trauma, vasoconstrictor mechanisms predominate and the endothelium becomes prothrombotic, procoagulatory and proinflammatory in nature. This is achieved by a reduction of endothelial dilating agents: adenosine, NO and prostacyclin; and by the direct action of ADP, serotonin and thromboxane on vascular smooth muscle cells to elicit their contraction (Becker et al. 2000). The chief trigger for the change in endothelial function that leads to the formation of a haemostatic thrombus is the loss of the endothelial cell barrier between blood and extracellular matrix components (Ruggeri 2002). Circulating platelets identify and discriminate areas of endothelial lesions; here, they adhere to the exposed sub endothelium. Their interaction with the various thrombogenic substrates and locally generated or released agonists results in platelet activation. This process is described as possessing two stages, firstly, adhesion - the initial tethering to a surface, and secondly aggregation - the platelet-platelet cohesion (Savage & Cattaneo et al. 2001). Three mechansism contribute to the loss of blood following vessel injury. The vessel constricts, reducing the loss of blood. Platelets adhere to the site of injury, become activated and aggregate with fibrinogen into a soft plug that limits blood loss, a process termed primary hemostasis. Proteins and small molecules are released from granules by activated platelets, stimulating the plug formation process. Fibrinogen from plasma forms bridges between activated platelets. These events initiate the clotting cascade (secondary hemostasis). Negatively-charged phospholipids exposed at the site of injury and on activated platelets interact with tissue factor, leading to a cascade of reactions that culminates with the formation of an insoluble fibrin clot. Edited: Joshi-Tope, G, 0000-00-00 00:00:00 |
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| ID |
http://purl.obolibrary.org/obo/HINO_0015199 |
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| comment |
Reviewed: Brummel, K, Rush, MG, Stafford, DW, 0000-00-00 00:00:00 Authored: D'Eustachio, P, Pace, N.P., Farndale, R, de Bono, B, 2004-01-21 22:18:59 Hemostasis is a physiological response that culminates in the arrest of bleeding from an injured vessel. Under normal conditions the vascular endothelium supports vasodilation, inhibits platelet adhesion and activation, suppresses coagulation, enhances fibrin cleavage and is anti-inflammatory in character. Under acute vascular trauma, vasoconstrictor mechanisms predominate and the endothelium becomes prothrombotic, procoagulatory and proinflammatory in nature. This is achieved by a reduction of endothelial dilating agents: adenosine, NO and prostacyclin; and by the direct action of ADP, serotonin and thromboxane on vascular smooth muscle cells to elicit their contraction (Becker et al. 2000). The chief trigger for the change in endothelial function that leads to the formation of a haemostatic thrombus is the loss of the endothelial cell barrier between blood and extracellular matrix components (Ruggeri 2002). Circulating platelets identify and discriminate areas of endothelial lesions; here, they adhere to the exposed sub endothelium. Their interaction with the various thrombogenic substrates and locally generated or released agonists results in platelet activation. This process is described as possessing two stages, firstly, adhesion - the initial tethering to a surface, and secondly aggregation - the platelet-platelet cohesion (Savage & Cattaneo et al. 2001). Three mechansism contribute to the loss of blood following vessel injury. The vessel constricts, reducing the loss of blood. Platelets adhere to the site of injury, become activated and aggregate with fibrinogen into a soft plug that limits blood loss, a process termed primary hemostasis. Proteins and small molecules are released from granules by activated platelets, stimulating the plug formation process. Fibrinogen from plasma forms bridges between activated platelets. These events initiate the clotting cascade (secondary hemostasis). Negatively-charged phospholipids exposed at the site of injury and on activated platelets interact with tissue factor, leading to a cascade of reactions that culminates with the formation of an insoluble fibrin clot. Edited: Joshi-Tope, G, 0000-00-00 00:00:00 |
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| definition source |
Pubmed11604561 Reactome, http://www.reactome.org Pubmed10798271 Pubmed12411949 |
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| label |
Hemostasis |
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| located_in | ||
| name |
Blood coagulation |
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| prefixIRI |
HINO:0015199 |
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| prefLabel |
Hemostasis |
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| seeAlso |
Reactome Database ID Release 43109582 GENE ONTOLOGYGO:0007596 ReactomeREACT_604 |
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| subClassOf | ||
| has_part |
http://purl.obolibrary.org/obo/HINO_0015305 http://purl.obolibrary.org/obo/HINO_0015307 http://purl.obolibrary.org/obo/HINO_0015311 http://purl.obolibrary.org/obo/HINO_0015297 http://purl.obolibrary.org/obo/HINO_0015219 |