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Related Concept Videos

Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

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...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

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...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

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.
Disorders of Hemostasis01:24

Disorders of Hemostasis

Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
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Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
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Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...

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Fatty acids in animals: thrombosis and hemostasis.

The American journal of clinical nutrition·1997
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Evaluation and management of the thrombosis-prone patient.

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What is the historical background of research on the role of fatty acids in thrombosis?

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Modulation of the fibrinolytic response of cultured human vascular endothelium by extracellularly generated oxygen radicals.

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Related Experiment Video

Updated: Jul 26, 2026

Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel
07:26

Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel

Published on: June 29, 2015

Stearic acid, clotting, and thrombosis

J C Hoak1

  • 1Division of Blood Diseases and Resources, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.

The American Journal of Clinical Nutrition
|December 1, 1994
PubMed
Summary

Stearic acid can cause blood clots by activating factor XII and aggregating platelets. Dietary stearic acid is unlikely to cause thrombosis in humans unless fatty acid transport is abnormal.

Area of Science:

  • Biochemistry
  • Hematology
  • Physiology

Background:

  • Stearic acid, a long-chain saturated fatty acid, has been implicated in blood coagulation.
  • The mechanisms by which fatty acids influence hemostasis are not fully understood.

Purpose of the Study:

  • To investigate the thrombogenic potential of stearic acid.
  • To elucidate the role of factor XII and platelet aggregation in stearic acid-induced hypercoagulability.
  • To determine the conditions under which stearic acid may pose a thrombotic risk in humans.

Main Methods:

  • Administration of unbound stearic acid (sodium salt) to dogs and birds.
  • Observation of hypercoagulability and thrombosis.
  • Investigation of the protective role of albumin binding.

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Ferric Chloride-Induced Arterial Thrombosis and Sample Collection for 3D Electron Microscopy Analysis

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Last Updated: Jul 26, 2026

Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel
07:26

Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel

Published on: June 29, 2015

Ferric Chloride-induced Murine Thrombosis Models
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Ferric Chloride-induced Murine Thrombosis Models

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Ferric Chloride-Induced Arterial Thrombosis and Sample Collection for 3D Electron Microscopy Analysis
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Ferric Chloride-Induced Arterial Thrombosis and Sample Collection for 3D Electron Microscopy Analysis

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  • Analysis of free fatty acid (FFA) to albumin molar ratios.
  • Main Results:

    • In dogs, stearic acid injection led to massive thrombosis and death, linked to factor XII activation and platelet aggregation.
    • Birds, deficient in factor XII, did not exhibit hypercoagulability or thrombosis.
    • Albumin binding of stearic acid at an FFA-albumin molar ratio < 2 prevented thrombotic effects.
    • No experimental evidence supports dietary stearic acid causing thrombosis in humans.

    Conclusions:

    • Stearic acid can induce hypercoagulability and thrombosis via factor XII and platelet activation.
    • Thrombotic risk in humans may arise from aberrant fatty acid transport, specifically elevated FFA-albumin molar ratios (>2).
    • Conditions like severe lipid mobilization or low albumin levels (e.g., nephrotic syndrome) could precipitate such risks.