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

Vascular Spasm01:16

Vascular Spasm

The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Inflammation01:38

Inflammation

Overview
Acute Inflammation III: Local and Systemic Effects01:25

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...
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...
Introduction to Hemostasis01:05

Introduction to Hemostasis

Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized, and...

You might also read

Related Articles

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

Sort by
Same author

Ethical responsibilities in clinical investigation.

Perspectives in biology and medicine·2015
Same author

ATHEROSCLEROSIS. COAGULATION MECHANISMS.

A listing of research in the cardiovascular field·2014
Same author

Carotid sinus syndrome in air crew personnel.

Bulletin of the U.S. Army Medical Department. United States. Army. Medical Department·2010
Same author

The coronary circulation.

Medicine·2010
Same author

THE LOCALIZED ACTION ON THE SPINAL CORD OF INTRAMUSCULARLY INJECTED TETANUS TOXIN.

The Journal of experimental medicine·2009
Same author

Confirmation of mendelian properties of heterodimeric fibrinogen molecules in a heterozygotic dysfibrinogenemia, "fibrinogen Amarillo," using gprphoresis to differentiate semifibrin molecules from fibrinogen and fibrin.

Thrombosis research·2001

Related Experiment Video

Updated: Jun 19, 2026

An in vivo Assay to Test Blood Vessel Permeability
07:03

An in vivo Assay to Test Blood Vessel Permeability

Published on: March 16, 2013

INCREASED VASCULAR PERMEABILITY INDUCED BY HUMAN PLASMIN.

O D Ratnoff1

  • 1Department of Medicine, Western Reserve University School of Medicine, and University Hospitals, Cleveland.

The Journal of Experimental Medicine
|October 30, 2009
PubMed
Summary

Plasminogen activation increases vascular permeability by producing kinins, a process inhibited by soybean trypsin inhibitor. This suggests plasmin

Area of Science:

  • Biochemistry
  • Physiology
  • Pharmacology

Background:

  • Vascular permeability is crucial for physiological processes.
  • The role of plasmin in modulating vascular permeability requires further elucidation.

Purpose of the Study:

  • To investigate the mechanism by which plasminogen activation affects vascular permeability.
  • To identify mediators involved in plasmin-induced permeability changes.

Main Methods:

  • In vivo experiments using guinea pig skin models.
  • Activation of plasminogen using streptokinase and urokinase.
  • Assays for vascular permeability and inhibition studies with soybean trypsin inhibitor and triprolidine.
  • Incubation of plasmin with plasma fractions rich in prokinin.

More Related Videos

High-Throughput Bioprinting Method for Modeling Vascular Permeability in Standard Six-well Plates with Size and Pattern Flexibility
07:41

High-Throughput Bioprinting Method for Modeling Vascular Permeability in Standard Six-well Plates with Size and Pattern Flexibility

Published on: August 16, 2024

Evaluating Vascular Hyperpermeability-inducing Agents in the Skin with the Miles Assay
08:43

Evaluating Vascular Hyperpermeability-inducing Agents in the Skin with the Miles Assay

Published on: June 19, 2018

Related Experiment Videos

Last Updated: Jun 19, 2026

An in vivo Assay to Test Blood Vessel Permeability
07:03

An in vivo Assay to Test Blood Vessel Permeability

Published on: March 16, 2013

High-Throughput Bioprinting Method for Modeling Vascular Permeability in Standard Six-well Plates with Size and Pattern Flexibility
07:41

High-Throughput Bioprinting Method for Modeling Vascular Permeability in Standard Six-well Plates with Size and Pattern Flexibility

Published on: August 16, 2024

Evaluating Vascular Hyperpermeability-inducing Agents in the Skin with the Miles Assay
08:43

Evaluating Vascular Hyperpermeability-inducing Agents in the Skin with the Miles Assay

Published on: June 19, 2018

Main Results:

  • Activated plasminogen significantly increased vascular permeability in guinea pigs.
  • This effect was dose-dependently inhibited by soybean trypsin inhibitor.
  • Triprolidine did not affect the permeability increase.
  • Plasmin incubation with prokinin-rich plasma fractions generated permeability-enhancing activity.

Conclusions:

  • Plasminogen activation enhances vascular permeability.
  • The mechanism involves the generation of kinins, likely mediated by plasmin.
  • Soybean trypsin inhibitor can block this effect, indicating a serine protease-dependent pathway.