Thromb Haemost 2004; 91(05): 1000-1008
DOI: 10.1160/TH03-08-0523
Endothelium and Vascular Development
Schattauer GmbH

Influence of low frequency electric fields on anti- and pro-coagulability of the vascular endothelium: new insights into high-voltage electrical injury

Dietmar Ulrich
1   Department of Plastic Surgery and Hand Surgery - Burn Center, University Hospital, Aachen University of Technology, Aachen, Germany
,
Norbert Pallua
1   Department of Plastic Surgery and Hand Surgery - Burn Center, University Hospital, Aachen University of Technology, Aachen, Germany
,
Franziska Lichtenegger
1   Department of Plastic Surgery and Hand Surgery - Burn Center, University Hospital, Aachen University of Technology, Aachen, Germany
,
Bernd Hafemann
1   Department of Plastic Surgery and Hand Surgery - Burn Center, University Hospital, Aachen University of Technology, Aachen, Germany
,
Jiri Silny
2   Research Center for Bioelectromagnetic Interaction (femu), Aachen University of Technology, Aachen, Germany
› Author Affiliations
Financial support: The work was supported by a grant from the Medical Faculty of Aachen University of Technology (START 12/2002).
Further Information

Publication History

Received 14 August 2003

Accepted after revision 07 January 2004

Publication Date:
01 December 2017 (online)

Summary

After high-voltage electric injury, patients often show tissue necrosis and thrombosis of blood vessels even remote from entry and exit site of electrical current. In this study, plasma levels of TAT, F1+2, PAI-1, and t-PA were determined in vivo in three patients with high-voltage injury for 96 hours after trauma. In order to analyse a possible effect on haemostasis related to endothelial cell damage, protein S, TF, ET-1, PGI2, NO, t-PA, and PAI-1 were determined for 72 hours in vitro in cell culture supernatant of HUVECs that had been exposed to 1, 10, 30, and 50 electric field periods of 50 Hz with field strength of 60 V/cm and duration of 20 ms. Furthermore, expression of thrombomodulin was immunohistochemically analysed. Clotting activation could be observed in our patients by increased levels of F1+2 and TAT between 12 and 72 hours after injury, whereas fibrinolysis was disturbed due to high PAI-1. One patient presented thrombosis of vessels by day 3. In vitro, PAI-1 increased significantly (p<0.05) in medium of cells with an application of 30 and 50 periods between 2 and 48 hours. Between 4 and 72 hours, the concentration of t-PA was significantly lower (p<0.05) in the medium of HUVECs exposed to 10, 30, and 50 periods, whereas there was a significant increase (p<0.05) in the concentration of TF in the cell groups with an application of 30 and 50 periods. 24, 48, and 72 hours after injury, there was just weak or no staining for thrombomodulin in HUVECs with an application of 30 and 50 periods. The disturbed balance between clotting system and fibrinolysis seen in vitro after electric injury might explain the clinical observation of a progressive thrombosis of blood vessels after electric injury leading to tissue loss.

 
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