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

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
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...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

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...
Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents01:24

Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents

In the intricate landscape of the gastric lumen, excessive acid secretion disrupts the natural defense mechanisms, weakening the mucus-bicarbonate barrier. This vulnerability allows pepsin to infiltrate epithelial cells, digesting mucosal proteins and triggering erosion, leading to ulcer formation.
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
Structure and Function of Platelets01:18

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...

You might also read

Related Articles

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

Sort by
Same author

Key Performance Indicators for Clinical Pharmacy Practice and Administration in Inpatient/Acute Care Settings: An Opinion of the Clinical Administration Practice and Research Network of the American College of Clinical Pharmacy.

Journal of the American College of Clinical Pharmacy : JACCP·2026
Same author

Improving weaning and liberation from mechanical ventilation for tracheostomy patients: a quality improvement initiative.

BMJ quality & safety·2025
Same author

Survey among Hospitals on Strategies to Ensure Appropriate Use of Intravenous Acetaminophen.

Hospital pharmacy·2024
Same author

Distinct Neural Profiles of Frontoparietal Networks in Boys with ADHD and Boys with Persistent Depressive Disorder.

Cognitive, affective & behavioral neuroscience·2022
Same author

Dissociable influences of reward and punishment on adaptive cognitive control.

PLoS computational biology·2021
Same author

Bedside medication delivery programs: suggestions for systematic evaluation and reporting.

International journal for quality in health care : journal of the International Society for Quality in Health Care·2019

Related Experiment Video

Updated: Jun 12, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Prasugrel, a new platelet inhibitor

Debbie Yee1, Joanne Meyer, Gina Caliendo

  • 1Mount Sinai Medical Center, New York, NY, USA. debbie.yee@mountsinai.org

The Mount Sinai Journal of Medicine, New York
|May 28, 2010
PubMed
Summary

No abstract available in PubMed .

More Related Videos

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
09:13

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation

Published on: April 6, 2017

Ferric Chloride-induced Murine Thrombosis Models
10:37

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

Related Experiment Videos

Last Updated: Jun 12, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
09:13

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation

Published on: April 6, 2017

Ferric Chloride-induced Murine Thrombosis Models
10:37

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016