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

Structure and Function of Platelets01:18

Structure and Function of Platelets

2.7K
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...
2.7K
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

8.5K
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...
8.5K
Introduction to Hemostasis01:05

Introduction to Hemostasis

12.8K
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,...
12.8K
Coagulation01:09

Coagulation

9.4K
The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
9.4K
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

8.2K
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
8.2K
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

11.6K
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
11.6K

You might also read

Related Articles

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

Sort by
Same author

Cyclooxygenase-1-Inhibition with Aspirin in Patients with Chronic Coronary Syndrome.

TH open : companion journal to thrombosis and haemostasis·2026
Same author

Association between Sex and Platelet Function in Patients with Diabetes Mellitus Type II: A Systematic Review.

Seminars in thrombosis and hemostasis·2026
Same author

Effects of Acute Exercise and 12-Week High-Intensity Interval Training on Inflammatory Biomarkers in Stable Coronary Artery Disease: A Randomized Controlled Trial.

Journal of the American Heart Association·2026
Same author

Apixaban Concentrations and Effects on Coagulation in Patients With Nephrotic Syndrome.

Kidney medicine·2025
Same author

Fibrinolytic Capacity and Risk of Bleeding in Intensive Care Patients with Acute Kidney Injury.

TH open : companion journal to thrombosis and haemostasis·2025
Same author

MicroRNA dynamics and their link to platelet function following acute ST-segment elevation myocardial infarction.

Thrombosis research·2025

Related Experiment Video

Updated: Jan 3, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

1.5K

Platelet function in patients with septic shock.

Mathies Appel Laursen1, Julie Brogaard Larsen1, Kim Michael Larsen2

  • 1Thrombosis & Haemostasis Research Unit, Department of Clinical Biochemistry, Aarhus University Hospital, Denmark.

Thrombosis Research
|November 23, 2019
PubMed
Summary
This summary is machine-generated.

Septic shock patients show normal platelet aggregation relative to platelet count, but increased platelet activation. Disseminated intravascular coagulation (DIC) did not further impair aggregation in these septic shock patients.

Keywords:
Disseminated intravascular coagulationPlatelet activationPlatelet aggregationPlatelet function testsSepsis

More Related Videos

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
09:38

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

14.3K
Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

959

Related Experiment Videos

Last Updated: Jan 3, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

1.5K
A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
09:38

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

14.3K
Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

959

Area of Science:

  • Hematology
  • Critical Care Medicine
  • Pathophysiology

Background:

  • Platelet function in sepsis-related disseminated intravascular coagulation (DIC) is not well understood.
  • Sepsis and DIC significantly impact patient outcomes, highlighting the need to investigate platelet behavior.

Purpose of the Study:

  • To evaluate platelet aggregation and activation in septic shock patients, independent of platelet count.
  • To compare platelet aggregation and activation between septic shock patients with and without DIC.

Main Methods:

  • Investigated 38 septic shock patients using impedance aggregometry and flow cytometry.
  • Assessed platelet aggregation relative to platelet count and measured markers of platelet activation (surface-bound fibrinogen, CD63, P-selectin).

Main Results:

  • Septic shock patients exhibited normal platelet aggregation relative to platelet count, even with DIC.
  • Increased platelet activation was observed in septic shock patients, indicated by higher platelet surface-bound fibrinogen and CD63.
  • Lower surface-bound P-selectin and higher plasma soluble P-selectin were noted in septic shock patients compared to controls.

Conclusions:

  • Septic shock does not impair platelet aggregation when adjusted for platelet count.
  • Platelet activation is significantly increased in septic shock patients, suggesting a prothrombotic state.
  • Further research is needed to elucidate the role of altered platelet activation in sepsis pathophysiology.