Sympathetic activation and inflammatory response in patients with subarachnoid haemorrhage
- 233 Downloads
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.
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.
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.
KeywordsSympathetic nervous system Norepinephrine Cytokines Complement
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.
- 11.Bürger A, Benicke M, Deten A, Zimmer HG (2001) Catecholamines stimulate interleukin-6 synthesis in rat cardiac fibroblasts. AJP Heart 281:14–21Google Scholar
- 18.Dilraj A, Botha JB, Rambiritch V, Miller R, van Dellen JR (1992) Levels of catecholamines in plasma and cerebrospinal fluid in aneurysmal subarachnoid hemorrhage. Neurosurg 31:42–51Google Scholar
- 20.Dampney R, Moon E (1980) Role of ventrolateral medulla in vasomotor response to cerebral ischemia. Am J Physiol 239:349–358Google Scholar
- 21.Reis D, Morrison S, Ruggiero D (1988) The C1 area of the brainstem in tonic and reflex control of blood pressure. Hypertension 11:18–23Google Scholar
- 24.Hidetoshi K, Takashi S (1989) Activated complement components C3a and C4a in cerebrospinal fluid and plasma following subarachnoid hemorrhage. J Neurosurg 71:741–746Google Scholar
- 25.Fassbender K, Hodapp B, Rossol S, Bertsch T, Schmeck J, Schutt S, Fritzinger M, Horn P, Vajkoczy P, Kreisel S, Brunner J, Schmiedek P, Hennerici M (2001) Inflammatory cytokines in subarachnoid haemorrhage: association with abnormal blood flow velocities in basal cerebral arteries Neurol Neurosurg Psychiatry 70:534–537Google Scholar
- 32.Esler M, Jennings G, Leonard P Sacharias N, Burke F, Johns J, Blombery P (1984) Contribution of individual organs to total noradrenaline release in humans. Acta Physiol Scand 527:11–16Google Scholar
- 35.Fassbender K, Rossol S, Kammer T, Daffertshofer M, Wirth S, Dollman M, Hennerici M (1994) Proinflammatory cytokines in serum of patients with acute cerebral ischemia: kinetics of secretion and relation to the extent of brain damage and outcome of disease. J Neurol Sci 122:135–139PubMedCrossRefGoogle Scholar