Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow01:26

Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow

Chronic liver disease significantly impacts drug metabolism due to alterations in hepatic blood flow and enzyme accessibility. This disruption affects the body's pharmacokinetics—the movement and processing of drugs within the system. Key enzymes crucial for metabolizing medications become less accessible, changing how drugs are processed and utilized. Furthermore, liver disease influences the synthesis of plasma proteins, such as albumin and globulins, which play critical roles in drug binding...
Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test01:22

Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test

In clinical practice, the direct measurement of hepatic blood flow to evaluate liver function presents significant challenges due to the intricate and specialized nature of the necessary techniques. Consequently, healthcare professionals often rely on empirical estimates derived from thorough patient examinations and liver function tests to gauge liver health. Among the tools at their disposal, the Child–Pugh and MELD scoring systems stand out for their ability to categorize and assess the...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Hyperammonemia in Hepatic Encephalopathy.

Journal of clinical and experimental hepatology·2018
Same author

Differential Response of Neural Cells to Trauma-Induced Swelling In Vitro.

Neurochemical research·2017
Same author

Role of Matricellular Proteins in Disorders of the Central Nervous System.

Neurochemical research·2016
Same author

Neuronal Cell Death Induced by Mechanical Percussion Trauma in Cultured Neurons is not Preceded by Alterations in Glucose, Lactate and Glutamine Metabolism.

Neurochemical research·2016
Same author

Sulfonylurea receptor 1 contributes to the astrocyte swelling and brain edema in acute liver failure.

Translational stroke research·2014
Same author

Brain edema in acute liver failure: role of neurosteroids.

Archives of biochemistry and biophysics·2013

Related Experiment Video

Updated: May 17, 2026

In vivo Liver Endocytosis Followed by Purification of Liver Cells by Liver Perfusion
12:35

In vivo Liver Endocytosis Followed by Purification of Liver Cells by Liver Perfusion

Published on: November 10, 2011

Endothelial-astrocytic interactions in acute liver failure.

A R Jayakumar1, M D Norenberg

  • 1Veterans Affairs Medical Center, Miami, FL, USA.

Metabolic Brain Disease
|October 27, 2012
PubMed
Summary

Brain edema in acute liver failure (ALF) involves astrocyte swelling. Recent findings suggest both cytotoxic and vasogenic mechanisms contribute to this dangerous neurological complication.

Area of Science:

  • Neurology
  • Hepatology
  • Pathology

Background:

  • Brain edema and increased intracranial pressure are critical neurological complications of acute liver failure (ALF).
  • Astrocyte swelling, a form of cytotoxic brain edema, is the primary neuropathological finding in ALF.
  • Emerging evidence indicates a potential interplay between cytotoxic and vasogenic mechanisms in ALF-associated brain edema.

Purpose of the Study:

  • To review the characteristics of brain edema in human and animal models of ALF.
  • To examine in vitro evidence supporting cytotoxic brain edema, specifically astrocyte swelling.
  • To elucidate the role of brain endothelial cells in astrocyte swelling and overall brain edema development in ALF.

Main Methods:

  • Literature review of studies on ALF-induced brain edema in humans and experimental animals.

More Related Videos

Long Term Intravital Multiphoton Microscopy Imaging of Immune Cells in Healthy and Diseased Liver Using CXCR6.Gfp Reporter Mice
11:44

Long Term Intravital Multiphoton Microscopy Imaging of Immune Cells in Healthy and Diseased Liver Using CXCR6.Gfp Reporter Mice

Published on: March 24, 2015

A Standardized Method for the Analysis of Liver Sinusoidal Endothelial Cells and Their Fenestrations by Scanning Electron Microscopy
08:38

A Standardized Method for the Analysis of Liver Sinusoidal Endothelial Cells and Their Fenestrations by Scanning Electron Microscopy

Published on: April 30, 2015

Related Experiment Videos

Last Updated: May 17, 2026

In vivo Liver Endocytosis Followed by Purification of Liver Cells by Liver Perfusion
12:35

In vivo Liver Endocytosis Followed by Purification of Liver Cells by Liver Perfusion

Published on: November 10, 2011

Long Term Intravital Multiphoton Microscopy Imaging of Immune Cells in Healthy and Diseased Liver Using CXCR6.Gfp Reporter Mice
11:44

Long Term Intravital Multiphoton Microscopy Imaging of Immune Cells in Healthy and Diseased Liver Using CXCR6.Gfp Reporter Mice

Published on: March 24, 2015

A Standardized Method for the Analysis of Liver Sinusoidal Endothelial Cells and Their Fenestrations by Scanning Electron Microscopy
08:38

A Standardized Method for the Analysis of Liver Sinusoidal Endothelial Cells and Their Fenestrations by Scanning Electron Microscopy

Published on: April 30, 2015

  • Analysis of in vitro research focusing on astrocyte cell swelling.
  • Examination of studies investigating the contribution of brain endothelial cells to edema.
  • Main Results:

    • Brain edema in ALF is characterized by significant astrocyte swelling.
    • In vitro studies confirm that astrocytes undergo swelling, supporting the cytotoxic edema model.
    • Brain endothelial cells play a documented role in the pathogenesis of astrocyte swelling and brain edema in ALF.

    Conclusions:

    • Brain edema in ALF likely involves both cytotoxic (astrocyte swelling) and vasogenic mechanisms.
    • Understanding the dual mechanisms is crucial for managing neurological complications in ALF.
    • Further research into the interaction between astrocytes and endothelial cells may reveal new therapeutic targets.