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Sympathetic activation and inflammatory response in patients with subarachnoid haemorrhage

Journal article
Authors Silvana Naredi
G. Lambert
Peter Friberg
Stefan Zäll
Elisabeth Edén
Bertil Rydenhag
Maria Tylman-Mikiewicz
Anders Bengtsson
Published in Intensive Care Med
Volume 32
Issue 12
Pages 1955-61
ISSN 0342-4642 (Print)
Publication year 2006
Published at Institute of Clinical Sciences, Department of Anesthesiology and Intensive care
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 1955-61
Language en
Links www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords Adult, Aged, Case-Control Studies, Cytokines/*blood, Female, Humans, Intensive Care Units, Male, Middle Aged, Norepinephrine/*blood, Subarachnoid Hemorrhage/*blood/immunology, Sympathetic Nervous System/immunology/metabolism
Subject categories Anaesthetics, Neurosurgery

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.

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