Related Experiment Video
Updated: Jul 21, 2026

06:39
An Optimized Evans Blue Protocol to Assess Vascular Leak in the Mouse
Published on: September 12, 2018
Isoprostanes induce plasma extravasation in rat skin
1Department of Anesthesiology, University of California, San Diego 92093, USA.
Prostaglandins & Other Lipid Mediators
|November 4, 2000
Summary
Isoprostanes E2 and F2 alpha promote skin inflammation and plasma leakage. This effect is largely independent of cyclooxygenase (COX) enzymes, suggesting novel mechanisms in inflammatory responses.
Area of Science:
- Biochemistry
- Pharmacology
- Dermatology
Background:
- Isoprostanes E2 (8-iso PGE) and F2 alpha (8-iso PGF) are implicated in vascular, inflammatory, and pain pathways.
- The precise mechanisms behind isoprostane actions remain under investigation.
Purpose of the Study:
- To investigate the role of isoprostanes in promoting cutaneous inflammation.
- To explore the involvement of cyclooxygenase (COX) pathways in isoprostane-induced plasma extravasation.
Main Methods:
- Utilized the Evan's blue dye method to assess plasma extravasation in rat skin.
- Administered 8-iso PGE and 8-iso PGF subcutaneously.
- Investigated the effects of COX inhibitors (ibuprofen and ketorolac) on isoprostane-induced responses.
Main Results:
- Subcutaneous injection of 8-iso PGE and 8-iso PGF induced plasma extravasation in glabrous rat skin.
- 8-iso PGE, but not 8-iso PGF, caused dye extravasation in hairy skin.
- Isoprostane-evoked plasma extravasation showed inconsistent reduction with COX inhibitors, unlike isoprostane-induced nociceptor sensitization.
Conclusions:
- A significant component of isoprostane-induced cutaneous plasma extravasation is independent of COX activity.
- These findings suggest COX-independent mechanisms contribute to isoprostane-mediated inflammation.
More Related Videos
Related Concept Videos
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Acute Inflammation III: Local and Systemic Effects
Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...

