Effect of active site-inactivated factor VIIa on ischaemia/reperfusion injury in a porcine flap model.

Research output: Contribution to journalArticle


In free flap surgery, restored blood flow following a lengthy ischaemic period may lead to necrosis as a result of ischaemia/reperfusion (IR) injury. This injury comprises both proinflammatory and prothrombotic events, where the tissue factor/factor VIIa complex probably has a key role. Active site-inactivated factor VIIa (FFR-rFVIIa) exerts an antithrombotic effect by binding to tissue factor without initiating coagulation. In this study we have evaluated the potential protective effects of FFR-rFVIIa in IR injury. Bilateral musculocutaneous latissimus dorsi flaps in 16 pigs were made ischaemic for eight hours, then given 1 mg/kg/flap of FFR-rFVIIa or vehicle intra-arterially, and reperfused for 10 hours. The viable:necrotic tissue ratio, and accumulation of radiolabelled leucocytes, fibrinogen, and platelets were measured. There was no effect on tissue survival, but radiolabelled components in viable tissue were increased, though not significantly so. We conclude that FFR-rFVIIa did not prevent IR injury, indicating that tissue factor-mediated coagulation is not an important determinant of IR injury in this setting.


  • Torbjörn Söderström
  • Lene Birk-Sørensen
  • Henrik Holst-Jensen
  • Ulla Hedner
  • Björn Arnljots
Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Clinical Medicine
  • Surgery


  • ischemia-reperfusion injury, coagulation, thrombosis prevention, free flaps
Original languageEnglish
Pages (from-to)326-334
JournalScandinavian Journal of Plastic and Reconstructive Surgery and Hand Surgery
Issue number6
Publication statusPublished - 2004
Publication categoryResearch

Bibliographic note

The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Emergency medicine/Medicine/Surgery (013240200), Reconstructive Surgery (013240300), Surgery Research Unit (013242220)