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Mathematical modeling of material-induced blood plasma coagulation.
Biomaterials. 2006 Feb; 27(5):796-806.B

Abstract

Contact activation of the intrinsic pathway of the blood coagulation cascade is initiated when a procoagulant material interacts with coagulation factor XII, (FXII) yielding a proteolytic enzyme FXIIa. Procoagulant surface properties are thought to play an important role in activation. To study the mechanism of interaction between procoagulant materials and blood plasma, a mathematical model that is similar in form and in derivation to Michaelis-Menten enzyme kinetics was developed in order to yield tractable relationships between dose (surface area and energy) and response (coagulation time (CT)). The application of this model to experimental data suggests that CT is dependent on the FXIIa concentration and that the amount of FXIIa generated can be analyzed using a model that is linearly dependent on contact time. It is concluded from these experiments and modeling analysis that the primary mechanism for activation of coagulation involves autoactivation of FXII by the procoagulant surface or kallikrein-mediated reciprocal activation of FXII. FXIIa-induced self-amplification of FXII is insignificant.

Authors+Show Affiliations

Department of Surgery, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

16099033

Citation

Guo, Zhe, et al. "Mathematical Modeling of Material-induced Blood Plasma Coagulation." Biomaterials, vol. 27, no. 5, 2006, pp. 796-806.
Guo Z, Bussard KM, Chatterjee K, et al. Mathematical modeling of material-induced blood plasma coagulation. Biomaterials. 2006;27(5):796-806.
Guo, Z., Bussard, K. M., Chatterjee, K., Miller, R., Vogler, E. A., & Siedlecki, C. A. (2006). Mathematical modeling of material-induced blood plasma coagulation. Biomaterials, 27(5), 796-806.
Guo Z, et al. Mathematical Modeling of Material-induced Blood Plasma Coagulation. Biomaterials. 2006;27(5):796-806. PubMed PMID: 16099033.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mathematical modeling of material-induced blood plasma coagulation. AU - Guo,Zhe, AU - Bussard,Karen M, AU - Chatterjee,Kaushik, AU - Miller,Rachel, AU - Vogler,Erwin A, AU - Siedlecki,Christopher A, Y1 - 2005/08/15/ PY - 2005/02/14/received PY - 2005/06/28/accepted PY - 2005/8/16/pubmed PY - 2006/1/13/medline PY - 2005/8/16/entrez SP - 796 EP - 806 JF - Biomaterials JO - Biomaterials VL - 27 IS - 5 N2 - Contact activation of the intrinsic pathway of the blood coagulation cascade is initiated when a procoagulant material interacts with coagulation factor XII, (FXII) yielding a proteolytic enzyme FXIIa. Procoagulant surface properties are thought to play an important role in activation. To study the mechanism of interaction between procoagulant materials and blood plasma, a mathematical model that is similar in form and in derivation to Michaelis-Menten enzyme kinetics was developed in order to yield tractable relationships between dose (surface area and energy) and response (coagulation time (CT)). The application of this model to experimental data suggests that CT is dependent on the FXIIa concentration and that the amount of FXIIa generated can be analyzed using a model that is linearly dependent on contact time. It is concluded from these experiments and modeling analysis that the primary mechanism for activation of coagulation involves autoactivation of FXII by the procoagulant surface or kallikrein-mediated reciprocal activation of FXII. FXIIa-induced self-amplification of FXII is insignificant. SN - 0142-9612 UR - https://www.unboundmedicine.com/medline/citation/16099033/Mathematical_modeling_of_material_induced_blood_plasma_coagulation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0142-9612(05)00593-4 DB - PRIME DP - Unbound Medicine ER -