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Related Concept Videos

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...
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...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

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.
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...
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...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

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 forms a...

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Related Experiment Video

Updated: Jun 10, 2026

Preparation and Pathogen Inactivation of Double Dose Buffy Coat Platelet Products using the INTERCEPT Blood System
12:40

Preparation and Pathogen Inactivation of Double Dose Buffy Coat Platelet Products using the INTERCEPT Blood System

Published on: December 7, 2012

Hemostatic function of buffy coat platelets in additive solution treated with pathogen reduction technology.

Sisse R Ostrowski1, Louise Bochsen, Nis A Windeløv

  • 1Section for Transfusion Medicine, Capital Region Blood Bank, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. sisse.ostrowski@gmail.com

Transfusion
|August 21, 2010
PubMed
Summary

Pathogen reduction technologies (PRTs) minimally impacted clot formation in stored platelets (PLTs). However, PRTs reduced PLT aggregation without red blood cells or plasma, an effect reversed by their addition.

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Treatment of Platelet Products with Riboflavin and UV Light: Effectiveness Against High Titer Bacterial Contamination
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Treatment of Platelet Products with Riboflavin and UV Light: Effectiveness Against High Titer Bacterial Contamination

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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

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Last Updated: Jun 10, 2026

Preparation and Pathogen Inactivation of Double Dose Buffy Coat Platelet Products using the INTERCEPT Blood System
12:40

Preparation and Pathogen Inactivation of Double Dose Buffy Coat Platelet Products using the INTERCEPT Blood System

Published on: December 7, 2012

Treatment of Platelet Products with Riboflavin and UV Light: Effectiveness Against High Titer Bacterial Contamination
10:32

Treatment of Platelet Products with Riboflavin and UV Light: Effectiveness Against High Titer Bacterial Contamination

Published on: August 24, 2015

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

Area of Science:

  • Transfusion Medicine
  • Hematology
  • Biotechnology

Background:

  • Pathogen reduction technologies (PRTs) are used to improve the safety of blood products.
  • The impact of PRTs on the hemostatic function of stored platelet concentrates is not fully understood.

Purpose of the Study:

  • To compare the hemostatic potential of stored buffy coat platelets (BCPs) with and without Mirasol PRT treatment.
  • To evaluate the influence of PRT on platelet function assays over extended storage periods.

Main Methods:

  • In vitro comparison of PRT-treated BCPs (PRT-BCP) and control BCPs (CON-BCP) up to 8 days of storage.
  • Hemostatic function assessed using thrombelastography (TEG) and impedance aggregometry (Multiplate).
  • Multiplate assays were performed with and without red blood cells (RBCs) and plasma.

Main Results:

  • PRT treatment minimally affected clot formation (TEG), with a slight reduction in maximum clot strength.
  • In the absence of RBCs and plasma, PRT-BCP showed significantly reduced aggregation across multiple agonists.
  • Addition of RBCs and plasma restored comparable aggregation levels in both PRT-BCP and CON-BCP.

Conclusions:

  • Mirasol PRT treatment has a minimal impact on overall clot formation in stored platelets.
  • Platelet aggregation is reduced by PRT in isolation but normalized with the addition of RBCs and plasma.
  • Further clinical trials are needed to determine the in vivo relevance of these findings for platelet function.