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2014, Number S2

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Rev Mex Anest 2014; 37 (S2)

Physiology of coagulation

Flores-Rivera OI, Ramírez-Morales K, Meza-Márquez JM, Nava-López JA

Language: Spanish
References: 15
Page: 382-386
PDF size: 243.56 Kb.


ABSTRACT

Hemostasis is the process that maintains the integrity of a closed, high-pressure circulatory system after vascular damage. For study purpose is divided into primary and secondary. Primary hemostasis refers to the processes by which the platelet plug is formed through adhesion, activation, secretion, and platelet aggregation. Secondary hemostasis involves activation of the enzyme system whose major objective is the formation of thrombin and fibrin for clot stabilization. Finally there is the process of fibrinolysis, which is responsible for removing the remains of the clot once repaired tissue damage. These systems under physiological conditions maintain a perfect balance and when lost, lead to a pathological condition, such as bleeding or thrombosis.


REFERENCES

  1. Davì G, Patrono C. Platelet activation and atherothrombosis. N Engl J Med. 2007;357:2482-2494.

  2. Furie B, Furie BC. Mechanisms of thrombus formation. N Engl J Med. 2008;359:938-949.

  3. Jennings LK. Mechanisms of platelet activation: need for new strategies to protect against platelet-mediated atherothrombosis. Thromb Haemost. 2009;102:248-257.

  4. Tselepis AD, Gerotziafas G, Andrikopoulos G, Anninos H, Vardas P. Mechanisms of platelet activation and modification of response to antiplatelet agents. Hellenic J Cardiol. 2011;52:128-140.

  5. Osaki T, Ichinose A. Current views of activating and regulatory mechanisms of blood coagulation. Nippon Rinsho. 2014;72(7):1206-1211.

  6. McMichael M. New models of hemostasis. Top Companion Anim Med. 2012;27:40-45.

  7. Hoffman M, Monroe DM. A cell-based model of hemostasis. Thromb Haemost. 2001;85:958-965.

  8. Lu G, Broze GJJ, Krishnaswamy S. Formation of factors IXa and Xa by the extrinsic pathway: differential regulation by tissue factor pathway inhibitor and antithrombin III. J Biol Chem. 2004;279:17241-17249.

  9. Wolberg AS. Thrombin generation and fibrin clot structure. Blood Rev. 2007;21:131-142.

  10. Jin RC, Voetsch B, Loscalzo J. Endogenous mechanisms of inhibition of platelet function. Microcirculation. 2005;12:247-258.

  11. Aleman MM, Walton BL, Byrnes JR, Wolberg AS. Fibrinogen and red blood cells in venous thrombosis. Thrombosis Research. 2014;133:S38-S40.

  12. Chapin JC, Hajjar KA. Fibrinolysis and the control of blood coagulation. Blood Rev. 2014. doi: 10.1016/j.blre.2014.09.003.

  13. Bajzar L, Manuel R, Nesheim ME. Purification and characterization of TAFI, a thrombin-activable fibrinolysis inhibitor. J Biol Chem. 1995;270:14477-14484.

  14. Huber K, Christ G, Wojta J, Gulba D. Plasminogen activator inhibitor type-1 in cardiovascular disease. Status report 2001. Thrombosis Research. 2001;103:S7-S19.

  15. Xiao Q, Danton MJ, Witte DP, Kowala MC, Valentine MT, Bugge TH, et al. Plasminogen deficiency accelerates vessel wall disease in mice predisposed to atherosclerosis. Proc Natl Acad Sci USA. 1997;94:10335-10340.




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