The Role of Factor XI in a Dilute Thromboplastin Assay of Extrinsic Coagulation Pathway

Rong He; Shilong Xiong; Xiaofan He; Fayi Liu; Jianzhong Han; Juncheng Li; Shilin He

doi:10.1055/s-0037-1615963

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 2001; 85(06): 1055-1059
DOI: 10.1055/s-0037-1615963

Review Article

Schattauer GmbH

The Role of Factor XI in a Dilute Thromboplastin Assay of Extrinsic Coagulation Pathway

Rong He

¹Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China

,

Shilong Xiong

¹Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China

,

Xiaofan He

¹Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China

,

Fayi Liu

¹Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China

,

Jianzhong Han

¹Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China

,

Juncheng Li

¹Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China

,

Shilin He

¹Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China

› Author Affiliations

Abstract

Summary

Blood coagulation has been thought to be composed of both intrinsic and extrinsic pathways. Recent evidence strongly supports the critical role of the extrinsic pathway in the initiation of blood coagulation. This investigation established an assay that examines the role of FXI in the thromboplastin-initiated (extrinsic) coagulation based on this new concept. Plasma clotting times were measured at different concentrations of thromboplastin with activated FXII inhibited (FXIIa-inhibited Diluted Thromboplastin Time, FXIIaiDTT). Only at low concentrations of thromboplastin was FXIIaiDTT of FXI-deficient plasma significantly prolonged than that of normal plasma. Depletion of FXI from normal plasma prolonged its FXIIaiDTT and replenishment of FXI shortened it. FXIIaiDTTs of both FVIII-deficient and FIX-deficient plasma were remarkably prolonged, and addition of normal plasma dose-dependently shortened it. Furthermore, earlier α-thrombin inhibition was directly correlated with decreasing FXa generation. The amount of FXa production was: platelet-rich plasma > platelet-poor plasma > FXI-deficient plasma. Therefore, our findings from the FXIIaiDTT assays not only support the critical role of extrinsic pathway in blood coagulation initiation, but also demonstrate the importance of FXI as an amplifier of thrombin generation in thromboplastin-initiated coagulation.

Key words

Blood coagulation - thromboplastin - factor VIII - factor IX - factor XI

Full Text

References

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