Related Experiment Video

Updated: Aug 12, 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

Eicosanoids in cirrhosis and portal hypertension

Yvonne Birney1, Eileen M Redmond, James V Sitzmann

  • 1School of Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland.

Prostaglandins & Other Lipid Mediators
|November 25, 2003
PubMed

Insights

Prostaglandin signaling is altered in portal hypertension and cirrhosis, affecting blood vessel function. Understanding these changes is key to managing liver disease complications.

Area of Science:

  • Hepatology
  • Vascular Biology
  • Biochemistry

Background:

  • Knowledge of portal hypertension and cirrhosis pathogenesis has advanced significantly.
  • Vasoactive systems are activated in portal hypertension, with endothelial factors like prostaglandins being crucial.
  • Prostaglandins are synthesized via the cyclooxygenase (COX) pathway from arachidonic acid.

Purpose of the Study:

  • To review the role of hormonal and hemodynamic factors in prostaglandin production in cirrhosis and portal hypertension.
  • To examine the consequences of altered prostaglandin signaling on liver and vascular structure and function.

Main Methods:

  • Review of recent literature on prostaglandin synthesis and signaling in liver disease.
  • Analysis of the interplay between hemodynamic forces and endothelial prostaglandin release.
  • Examination of changes in intrahepatic and peripheral vascular resistance.

Main Results:

  • Altered hemodynamic profiles in portal hypertension influence endothelial release of vasoactive substances.
  • Prostaglandins are released from endothelium in response to humoral and mechanical stimuli.
  • Intrahepatic resistance is affected by reduced sinusoidal vasodilator responsiveness and increased vasoconstrictor prostanoid responsiveness.

Conclusions:

  • Hormonal and hemodynamic changes significantly impact prostaglandin production and signaling in cirrhosis and portal hypertension.
  • These alterations contribute to structural and functional changes in the vasculature and liver.
  • Further research into prostaglandin pathways may offer therapeutic targets for portal hypertension.

More Related Videos

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats09:37

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats

Published on: August 1, 2018

Measurement of the Hepatic Venous Pressure Gradient and Transjugular Liver Biopsy07:10

Measurement of the Hepatic Venous Pressure Gradient and Transjugular Liver Biopsy

Published on: June 18, 2020

Related Concept Videos

Esophageal Varices-I: Introduction01:24

Esophageal Varices-I: Introduction

Esophageal varices are dilated, tortuous veins which are found mainly in the submucosa of the lower esophagus but which may also appear higher up or extend into the stomach. They develop due to increased pressure in the portal venous system, often as a result of liver cirrhosis. This condition scars and damages the liver, impeding normal blood flow through the portal vein. To compensate, blood seeks alternative pathways, forming fragile new vessels (varices) in the esophagus and stomach. These...
Esophageal Varices-II: Clinical Features and Management01:28

Esophageal Varices-II: Clinical Features and Management

Esophageal varices often manifest as gastrointestinal bleeding episodes, presenting symptoms like hematemesis (vomiting of blood), hematochezia (passing fresh blood via the rectum), and melena (black, tarry stools). Other signs can include weight loss, anorexia, abdominal discomfort, jaundice, pruritus, altered mental status, and muscle cramps.
In the initial assessment, a thorough review of the patient's medical history is vital to identify risk factors such as liver disease, alcohol abuse, or...
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Cirrhosis I: Introduction01:23

Cirrhosis I: Introduction

Cirrhosis is a chronic, irreversible liver disease characterized by the widespread replacement of healthy liver tissue with fibrotic scar tissue and the formation of regenerative nodules.Etiology of cirrhosisCirrhosis results from sustained liver injury that triggers progressive fibrosis and structural remodeling. The underlying causes are diverse, encompassing common and less frequent clinical conditions. Regardless of the origin, all causes lead to chronic inflammation, hepatocyte loss, and...
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...
Portal Hypertension01:22

Portal Hypertension

Portal hypertension is an increase in blood pressure within the portal venous system. Normally, this pressure is less than 5 mmHg. It is considered clinically significant when it rises above 10 mmHg. At this threshold, complications from altered blood flow and venous congestion emerge.EtiologyPortal hypertension arises from conditions that impede blood flow through the liver. The most common cause is cirrhosis, in which chronic liver injury leads to fibrotic scarring. This fibrosis narrows or...