Volume 17 Supplement 2

Danish Society for Emergency Medicine: Research Symposium 2009

Open Access

Cerebral net exchange of Brain-Derived Neurotrophic Factor (BDNF) during experimental systemic inflammation and hypoxaemia in humans

  • Ronan MG Berg1Email author,
  • Sarah Taudorf1,
  • Damian M Bailey2,
  • Carsten Lundby3,
  • Bente Klarlund Pedersen1, 3 and
  • Kirsten Møller1, 4
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine200917(Suppl 2):P6

DOI: 10.1186/1757-7241-17-S2-P6

Published: 20 August 2009

Sepsis is notably associated with neuronal damage, an effect that may be exacerbated by hypoxaemia. The present study was designed to investigate if this interrelationship involves an effect on brain-derived neurotrophic factor (BDNF), an intrinsic neuroprotective agent which is released from the brain under normophysiological conditions [1]. We hypothesised that experimental systemic inflammation and hypoxaemia would abolish this release.

36 healthy male volunteers aged 25 (SD, 4) years were randomised to:
  1. 1.

    normoxia for 12 hours and a four-hour intravenous infusion of lipopolysaccharide (LPS) from 4–8 h (total dose 0.3 ng/kg), N = 12

     
  2. 2.

    hypoxia for 12 hours (12.9% O2) and a four-hour intravenous infusion of saline from 4–8 h, N = 11

     
  3. 3.

    hypoxia for 12 hours (12.9% O2) and a four-hour intravenous infusion of LPS from 4–8 h (total dose of 0.3 ng/kg), N = 13

     

Cerebral blood flow (CBF) was measured by the Kety-Schmidt technique, and arterio-jugular venous concentrations of BDNF were determined at baseline and 9 h. The cerebral net exchange was calculated by multiplying CBF with the arterio-jugular concentration differences of BDNF.

A cerebral release of BDNF was present at baseline (P < 0.005). This was attenuated in all three groups, but with no difference in the cerebral net exchange values from baseline or between interventions (NS, MANOVA). There was no effect of any of the interventions on the arterial levels of BDNF (NS, MANOVA).

In conclusion, systemic inflammation and hypoxaemia may abolish the net cerebral release of BDNF in healthy humans.

Authors’ Affiliations

(1)
Centre of Inflammation and Metabolism, Department of Infectious Diseases, University Hospital Rigshospitalet
(2)
Neurovascular Research Laboratory, Faculty of Health and Science, University of Glamorgan
(3)
Copenhagen Muscle Research Centre, Rigshospitalet, University of Copenhagen
(4)
Departments of Cardiothoracic Anesthesia and Intensive Care Unit 4131, University Hospital Rigshospitalet

References

  1. Krabbe KS et al.: Diabetologia. 2007, 50 (2): 431-8. 10.1007/s00125-006-0537-4.View ArticlePubMedGoogle Scholar

Copyright

© Berg et al; licensee BioMed Central Ltd. 2009

This article is published under license to BioMed Central Ltd.

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