Antibody inhibition of contact factor XII reduces platelet deposition in a model of extracorporeal membrane oxygenator perfusion in nonhuman primates.

ABSTRACT:

Background

The contact factor XII (FXII) activates upon contact with a variety of charged surfaces. Activated FXII (FXIIa) activates factor XI, which activates factor IX, resulting in thrombin generation, platelet activation, and fibrin formation. In both in vitro and in vivo rabbit models, components of medical devices, including extracorporeal oxygenators, are known to incite fibrin formation in a FXII-dependent manner. Since FXII has no known role in hemostasis and its inhibition is therefore likely a safe antithrombotic approach, we investigated whether FXII inhibition also reduces accumulation of platelets in extracorporeal oxygenators.

Objectives

We aimed to determine the effect of FXII inhibition on platelet deposition in perfused extracorporeal membrane oxygenators i

SUBMITTER: Wallisch M 

PROVIDER: S-EPMC7040549 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature