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...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Peripheral Artery Disease III: Interprofessional Care01:27

Peripheral Artery Disease III: Interprofessional Care

Peripheral Artery Disease (PAD) is characterized by narrowed arteries that diminish blood flow to the extremities. Effective management of PAD requires an interprofessional approach involving various healthcare professionals. The critical aspects of interprofessional care for PAD patients focus on risk factor modification, drug therapy, exercise therapy, nutrition therapy, critical limb ischemia care, and interventional radiology and surgical procedures.The primary treatment goal for PAD...
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...

You might also read

Related Articles

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

Sort by
Same author

From the ASPREE investigators: Response to Wittes et al.

Clinical trials (London, England)·2025
Same author

Robotic Stroke Thrombectomy: A Feasibility and Efficacy Study in Flow Models.

Journal of stroke·2025
Same author

Persistent Tissue-Level Hypoperfusion (No-Reflow) Negates the Clinical Benefit of Successful Thrombectomy.

Stroke·2025
Same author

Submaximal Angioplasty for Severe Intracranial Atherosclerotic Stenosis: Benefit of Revascularization at Last.

Stroke·2025
Same author

Costs and Benefits of the Melbourne Mobile Stroke Unit Compared With Standard Ambulance: Causal Analysis Using Observational Linked Data.

Stroke·2025
Same author

Efficacy and safety of intravenous alteplase for unknown onset stroke on prior antiplatelet therapy: Post hoc analysis of the EOS individual participant data.

International journal of stroke : official journal of the International Stroke Society·2025
Same journal

Management of Patients at Risk of Ischemic Stroke With Left Ventricular Systolic Dysfunction in the Absence of Intracardiac Thrombus: A Scientific Statement From the American Heart Association.

Stroke·2026
Same journal

Update on Rehabilitation After Stroke: Global Changes and the Continued Importance of Therapy Intensity, Dose, and Timing.

Stroke·2026
Same journal

ENTF Neuromodulation Yields Reduced Disability After Stroke: An Individual Participant-Level Data Meta-Analysis.

Stroke·2026
Same journal

Menopause and Its Implications for Stroke in Women.

Stroke·2026
Same journal

Physician Approaches to Determining Goals of Stroke Care for Patients Living With Disability or Dementia: Results from the SEED Mixed-Methods Study.

Stroke·2026
Same journal

Aspirin for Stroke Primary Prevention: A Step Toward Genetic-Driven Personalized Medicine.

Stroke·2026
See all related articles

Related Experiment Video

Updated: Jun 23, 2026

Ferric Chloride-induced Murine Thrombosis Models
10:37

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

Antiplatelet activity

Stephen M Davis1, Geoffrey A Donnan

  • 1Royal Melbourne Hospital, University of Melbourne, Parkville, Victoria, Australia. stephen.davis@mh.org.au

Stroke
|May 2, 2009
PubMed
Summary

No abstract available in PubMed .

More Related Videos

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor
06:32

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor

Published on: May 2, 2025

Related Experiment Videos

Last Updated: Jun 23, 2026

Ferric Chloride-induced Murine Thrombosis Models
10:37

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor
06:32

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor

Published on: May 2, 2025