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Related Concept Videos

Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
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...
Venous Thrombosis I: Introduction01:30

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...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
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.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.

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Related Experiment Video

Updated: Jul 13, 2026

Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model
05:12

Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model

Published on: September 4, 2017

Thrombotic molecule expression in cerebral vascular malformations.

Kingsley P Storer1, Jian Tu, Athula Karunanayaka

  • 1Prince of Wales Medical Research Institute, University of New South Wales, Sydney, New South Wales, Australia.

Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia
|July 25, 2007
PubMed
Summary

Radiosurgery can cause endothelial damage in arteriovenous malformations (AVMs), exposing tissue factor and potentially leading to thrombosis. Long-term changes in thrombotic molecule expression were not observed after treatment.

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Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel
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Published on: June 29, 2015

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Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model
05:12

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Published on: September 4, 2017

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

Area of Science:

  • Vascular Surgery
  • Oncology
  • Pathology

Background:

  • Thrombosis is a critical factor in the success of radiosurgery for vascular malformations.
  • Understanding thrombotic molecule expression in AVMs and CMs is crucial for treatment optimization.

Purpose of the Study:

  • To investigate thrombotic molecule expression in AVMs and CMs.
  • To analyze changes in AVMs following radiosurgery.

Main Methods:

  • Immunofluorescence analysis of tissue factor, thrombomodulin, and von Willebrand factor (vWF).
  • Study included 18 AVMs, 7 CMs, and 3 control specimens.
  • Examined AVMs treated with radiosurgery or embolization.

Main Results:

  • Thrombomodulin and vWF were expressed in the endothelium of all specimens.
  • Tissue factor was primarily located in the perivascular region and adventitia.
  • Irradiated AVMs showed loss of endothelial vWF and exposed tissue factor.

Conclusions:

  • Endothelial loss and tissue factor exposure occur in irradiated AVMs.
  • No significant long-term alterations in thrombotic molecule expression were observed post-radiosurgery.
  • Further research is needed to understand the immediate response to irradiation.