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Intensive Care Medicine

, Volume 32, Issue 12, pp 1955–1961 | Cite as

Sympathetic activation and inflammatory response in patients with subarachnoid haemorrhage

  • Silvana NarediEmail author
  • Gavin Lambert
  • Peter Friberg
  • Stefan Zäll
  • Elisabeth Edén
  • Bertil Rydenhag
  • Maria Tylman
  • Anders Bengtsson
Original

Abstract

Objective

The aim of this study was to evaluate the correlation between sympathetic nervous activation and the immune response in patients following subarachnoid haemorrhage (SAH).

Design and setting

Clinical study in a neurosurgical intensive care unit.

Patients and participants

Fourteen patients with acute non-traumatic SAH were included. Fifteen healthy, age-matched volunteers served as controls for measurement of catecholamine spillover.

Intervention

Blood sampling for C3a, C5b-9, IL-6, IL-8 and norepinephrine kinetic determination was made within 48 h, at 72 h and on the 7th–10th day after the SAH.

Measurements and results

SAH patients exhibited a profound increase in the rate of norepinephrine spillover to plasma at 48 h, 72 h and 7–10 days after the insult, 3–4 times that in healthy individuals. The plasma levels of C3a, IL-6 and C5b-9 were significantly elevated at 48 h, at 72 h and 7–10 days after the SAH, but the plasma level of IL-6 decreased significantly 7–10 days after the SAH. There was no relationship between the magnitude of sympathetic activation and the levels of inflammatory markers.

Conclusions

Following SAH a pronounced activation of the sympathetic nervous system and the inflammatory system occurs. The lack of significant association between the rate of spillover of norepinephrine to plasma and the plasma levels of inflammatory markers indicates that the two processes, sympathetic activation and the immune response, following SAH are not quantitatively linked. In spite of a persistent high level of sympathetic activation the plasma level of IL-6 decreased significantly one week after SAH.

Keywords

Sympathetic nervous system Norepinephrine Cytokines Complement 

Notes

Acknowledgements

This study was performed at Sahlgrenska University Hospital, Göteborg, Sweden. The study was supported by grants from the Regional Health Care Authority of West Sweden, The Göteborg Medical Society, the Swedish Society of Medicine, the Swedish Medical Research Council and the National Health and Medical Council of Australia.

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Copyright information

© Springer-Verlag 2006

Authors and Affiliations

  • Silvana Naredi
    • 1
    Email author
  • Gavin Lambert
    • 2
    • 3
  • Peter Friberg
    • 2
  • Stefan Zäll
    • 4
  • Elisabeth Edén
    • 4
  • Bertil Rydenhag
    • 5
  • Maria Tylman
    • 4
  • Anders Bengtsson
    • 4
  1. 1.Department of Anaesthesiology and Intensive CareUmeå University HospitalUmeåSweden
  2. 2.Department of Clinical PhysiologySahlgrenska University HospitalGöteborgSweden
  3. 3.Baker Heart Research InstituteMelbourneAustralia
  4. 4.Department of Anaesthesiology and Intensive CareSahlgrenska University HospitalGöteborgSweden
  5. 5.Department of NeurosurgerySahlgrenska University HospitalGöteborgSweden

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