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(Stroke. 2000;31:901.)
© 2000 American Heart Association, Inc.

Original Contributions

Increased Sympathetic Nervous Activity in Patients With Nontraumatic Subarachnoid Hemorrhage

S. Naredi, MD; G. Lambert, PhD; E. Edén, MD, PhD; S. Zäll, MD, PhD; M. Runnerstam, MD; B. Rydenhag, MD, PhD P. Friberg, MD, PhD

From the Department of Anaesthesiology and Intensive Care (S.N., E.E., S.Z.), Institute of Surgical Sciences; the Department of Neurosurgery (M.R., B.R.), Institute of Clinical Neurosciences; and the Department of Clinical Physiology (G.L., P.F.), Sahlgrenska University Hospital, Göteborg, Sweden.

Correspondence to Silvana Naredi, MD, Department of Anaesthesiology and Intensive Care, Umeå University Hospital, S-901 85 Umeå, Sweden. E-mail Peter.Naredi{at}surgery.umu.se

Background and Purpose—Activation of the sympathetic nervous system, which leads to elevation of circulating catecholamines, is implicated in the genesis of cerebral vasospasm and cardiac aberrations after subarachnoid hemorrhage. To this juncture, sympathetic nervous testing has relied on indirect methods only.

Methods—We used an isotope dilution technique to estimate the magnitude and time course of sympathoadrenal activation in 18 subarachnoid patients.

Results—Compared with 2 different control groups, the patients with subarachnoid hemorrhage exhibited an approximately 3-fold increase in total-body norepinephrine spillover into plasma within 48 hours after insult (3.2±0.3 and 4.2±0.7 versus 10.2±1.4 nmol/L; P<0.05 versus both). This sympathetic activation persisted throughout the 7- to 10-day examination period and was normalized at the 6-month follow-up visit.

Conclusions—The present study has established that massive sympathetic nervous activation occurs in patients after subarachnoid hemorrhage. This overactivation may relate to the well-known cardiac complications described in subarachnoid hemorrhage.

Key Words: norepinephrine • subarachnoid hemorrhage • sympathetic nervous system

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