(Stroke. 1999;30:1955-1961.)
© 1999 American Heart Association, Inc.
Original Contributions |
Effects of S-Nitrosoglutathione on Acute Vasoconstriction and Glutamate Release After Subarachnoid Hemorrhage
From the Department of Neurosurgery, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY.
Correspondence to Joshua B. Bederson, MD, Department of Neurosurgery, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1136, New York, NY 10029-6574. E-mail jbederson{at}mssm.edu
Background and Purpose—Subarachnoid hemorrhage (SAH) causes acute vasoconstriction that contributes to ischemic brain injury shortly after the initial bleed. It has been theorized that decreased availability of nitric oxide (NO) may contribute to acute vasoconstriction. Therefore we examined the effect of the NO donor N-nitroso glutathione (GSNO) on acute vasoconstriction and early ischemic glutamate release after experimental SAH.
Methods—SAH was induced by the endovascular suture method in anesthetized rats. GSNO (1 µmol/L/kg, n=31) or saline (n=21) was injected 5 minutes after SAH. Sham-operated rats received GSNO (1 µmol/L/kg, n=5) 5 minutes after sham surgery. Arterial and intracranial pressures, cerebral blood flow (CBF), and extracellular glutamate release were measured serially for 60 minutes after SAH. SAH size was determined, and vascular measurements were made histologically.
Results—GSNO had no effect on resting blood pressure, intracranial pressure, cerebral perfusion pressure, or CBF in sham-operated animals. However, administration of GSNO after SAH was associated with significantly increased CBF (161.6±26.6% versus saline 37.1±5.5%, 60 minutes after SAH, P<0.05), increased blood vessel diameter (internal carotid artery [ICA] 285.0±16.5 µm versus saline 149.2±14.1 µm, P<0.01), decreased vessel wall thickness (ICA12.9±0.7 µm versus saline 25.1±1.6 µm, P<0.01), and decreased extracellular glutamate levels (3315.6±1048.3% versus saline469.7±134.3%, P<0.05). Blood pressure decreased transiently, whereas intracranial pressure, cerebral perfusion pressure, and SAH size were not affected.
Conclusions—These results suggest that GSNO can reverse acute vasoconstriction and prevent ischemic brain injury after SAH. This further implies that acute vasoconstriction contributes significantly to ischemic brain injury after SAH and is mediated in part by decreased availability of NO.
Editorial Comment
Department of Neurosurgery, University of California, Davis, Sacramento, California
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