• L E Pelinka, L Szalay, M Jafarmadar, R Schmidhammer, H Redl, and S Bahrami.
• Ludwig Boltzmann Institute of Experimental and Clinical Traumatology and Research Unit of the Workers' Compensation Board (AUVA), Donaueschingenstrasse 13, A-1200 Vienna, Austria. lindapel@via.at
• Br J Anaesth. 2003 Oct 1; 91 (4): 595-7.

BackgroundS100B is an acknowledged marker of brain damage. However, trauma without brain damage also causes an increase in S100B. S100B concentrations are highest in multiple trauma patients with long bone fractures. Clinically, extensive long bone fractures are associated with haemorrhagic shock and haemorrhagic shock per se is associated with increased S100B. The aim of our experimental study was to verify the S100B increase in long bone fracture without haemorrhagic shock.Methodsand results. Bilateral femur fracture was carried out in 10 anaesthetized rats. Blood samples were drawn for immuno-luminometrical S100B measurement 5, 15, 30, 120, and 240 min after fracture. Mean arterial pressure (MAP), heart rate, and body temperature were monitored continuously. S100B increased after bilateral femur fracture and reached a peak 30-120 min after fracture (P<0.001). MAP remained at a level which is not associated with shock in rats. Heart rate and body temperature remained unchanged. Autopsy verified open bilateral femur fracture surrounded only by small zones of clotted blood.ConclusionsS100B is increased in bilateral femur fracture without haemorrhagic shock in rats. This finding suggests that bone marrow is a potential extracerebral source of S100B.

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