procoagulant


Also found in: Medical, Encyclopedia, Wikipedia.

pro·co·ag·u·lant

 (prō′kō-ăg′yə-lənt)
n.
1. The precursor of any of various blood factors necessary for coagulation.
2. An agent that promotes the coagulation of blood.
References in periodicals archive ?
Procoagulant FVa is deactivated by APC with an initial cleavage of the FVa peptide at the [Arg.
The procoagulant potential of environmental particles (PM10).
6,7 Thromboembolic disease in haematological malignancies is complex and can result from various factors such as tumour cell-derived procoagulant, fibrinolytic or proteolytic factors, inflammatory cytokines, chemotherapy and anti-angiogenic drugs increase this phenomenon.
While inflammatory events increase procoagulant factors, they decrease natural anticoagulants and fibrinolytic activity (38).
Platelets promote hemostasis by four interconnected mechanisms: adhesion to the sites of vascular injury; cellular activation and release of granule contents; aggregation, recruitment and amplification to form a hemostatic platelet plug; and providing a procoagulant phospholipid surface.
A shortened TEG r time reflects an increase in procoagulant activity, an increased alpha angle reflects an increased rate of thrombin generation, and an increased maximal amplitude reflects greater interaction between fibrinogen and platelets (6).
For one, they postulated that the "balance between procoagulant and anticoagulant factors in cirrhotics shifts to favor the latter with increasing age.
OBJECTIVES: We investigate the procoagulant activation of erythrocytes, an important contributor to thrombosis, by low-level mercury to explore the roles of erythrocytes in mercury-related cardiovascular diseases.
It is likely that a combination of factors is responsible for tilting the scale in favour of the procoagulant state in individuals infected by HIV.
The major effect of the procoagulant inhibitors, antithrombin (AT), activated protein C (APC), and tissue factor pathway inhibitor (TFPI) on inflammation is to:
Because transdermal menopausal estrogen therapy does not increase hepatic production of procoagulant factors, as does oral estrogen, it is biologically plausible that transdermal therapy is safer than oral therapy in terms of the risk of VTE.
The investigators studied procoagulant, anticoagulant, and fibrinolytic markers in blood samples that were taken at the time the women entered the WHI studies.