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Anticoagulant Drugs: Low-Molecular-Weight Heparins

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...

Formation of the Platelet Plug

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The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...

Clot Retraction and Fibrinolysis

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After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.

Extrinsic and Intrinsic Pathways of Hemostasis

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Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...

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Platelet activation and endogenous thrombin potential in pre-eclampsia.

M G Macey¹, S Bevan, S Alam

¹Department of Haematology, Barts and the London NHS Trust, London, UK. marion.macey@bartsandthelondon.nhs.uk

Thrombosis Research

|October 14, 2009

Summary

Pre-eclampsia involves platelet and coagulation activation. This study found significantly higher levels of activated platelets and platelet aggregates in women with pre-eclampsia compared to pregnant controls.

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Area of Science:

Obstetrics and Gynecology
Hematology
Pathophysiology

Background:

Platelets and the coagulation system are implicated in pre-eclampsia pathogenesis.
Previous research suggests a potential role for these systems in the condition.

Purpose of the Study:

To investigate elevated platelet and coagulation activation markers in pre-eclampsia.
To compare activation markers between pre-eclamptic, normotensive pregnant, and non-pregnant women.

Main Methods:

A case-control study design was employed.
Flow cytometry assessed activated platelets, platelet-monocyte/neutrophil aggregates, and platelet microparticles.
Calibrated Automated Thrombogram system measured thrombin generation capacity markers: endogenous thrombin potential (ETP), peak height, lag time, and time to peak.

Main Results:

Women with pre-eclampsia showed significantly higher percentages of CD62P+ platelets, CD62P+ platelet microparticles, and platelet-monocyte aggregates compared to pregnant controls.
Both pregnant groups exhibited significantly higher ETP and peak height than non-pregnant women.
Women with pre-eclampsia had significantly higher ETP and peak height than normotensive pregnant controls.

Conclusions:

This study provides comprehensive laboratory evidence of both platelet and coagulation activation in pre-eclampsia.
Findings support the involvement of these systems in the pathophysiology of pre-eclampsia.