Related Experiment Video

Updated: Aug 4, 2026

In Vitro and In Vivo Model to Study Bacterial Adhesion to the Vessel Wall Under Flow Conditions
10:24

In Vitro and In Vivo Model to Study Bacterial Adhesion to the Vessel Wall Under Flow Conditions

Published on: June 11, 2015

Fibrinogen binding and platelet retention: relationship with the thrombogenicity of catheters

A L Bailly1, A Laurent, H Lu

  • 1Laboratory of Neuroradiology and Therapeutic Angiography, Faculté de Médecine Lariboisière-St Louis, Paris, France.

Journal of Biomedical Materials Research
|January 1, 1996
PubMed

Insights

Catheter thrombogenicity, a risk for blood clots, was assessed by measuring fibrinogen binding and platelet retention. Higher fibrinogen binding and platelet retention indicate greater catheter thrombogenicity, aiding in preclinical testing.

Area of Science:

  • Biomaterials Science
  • Medical Device Engineering
  • Hematology

Background:

  • Catheter use poses thrombogenicity risks, potentially leading to dangerous clot embolization.
  • Evaluating catheter thrombogenicity is crucial for preventing patient harm.

Purpose of the Study:

  • To compare the in vivo thrombogenicity of four angiography catheters.
  • To assess in vitro fibrinogen binding and platelet retention as predictors of thrombogenicity.

Main Methods:

  • In vivo thrombogenicity evaluated by blood flow rate reduction in angiographic conditions.
  • In vitro fibrinogen and von Willebrand factor binding assessed via direct-ELISA.
  • In vitro platelet retention studied using 111Indium-labelled platelets.

Main Results:

  • Fibrinogen binding and platelet retention correlate well with catheter thrombogenicity.
  • Fibrinogen binding is a superior predictor compared to platelet retention.
  • Albumin precoating proved ineffective in preventing fibrinogen deposition.

Conclusions:

  • Fibrinogen deposition and platelet retention are valuable metrics for preclinical catheter evaluation.
  • Understanding catheter thrombogenicity is key to improving medical device safety.

More Related Videos

Characterization of Leukocyte-platelet Rich Fibrin, A Novel Biomaterial08:14

Characterization of Leukocyte-platelet Rich Fibrin, A Novel Biomaterial

Published on: September 29, 2015

Hemocompatibility Testing of Blood-Contacting Implants in a Flow Loop Model Mimicking Human Blood Flow09:41

Hemocompatibility Testing of Blood-Contacting Implants in a Flow Loop Model Mimicking Human Blood Flow

Published on: March 5, 2020

Related Concept Videos

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...
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...
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...
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.
Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
Venous Thrombosis III: Interprofessional Care01:29

Venous Thrombosis III: Interprofessional Care

Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...