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(Stroke. 2006;37:1314.)
© 2006 American Heart Association, Inc.

Original Contributions

Hyperbaric Oxygen Suppresses NADPH Oxidase in a Rat Subarachnoid Hemorrhage Model

From the Department of Physiology and Pharmacology (R.P.O., J.T., J.H.Z.), Division of Neurosurgery, the Department of Surgery (J.H.Z.), and the Department of Anesthesiology (J.H.Z.), Loma Linda University, Loma Linda, Calif.

Correspondence to John H. Zhang, MD, PhD, Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Risley Hall Room 223, Loma Linda, CA 92354. E-mail johnzhang3910{at}yahoo.com

Background and Purpose— One of the major contributors to brain injury after subarachnoid hemorrhage (SAH) is oxidative stress, and 1 of the major enzymatic sources of superoxide anion production in the brain is NADPH oxidase. Therefore, we studied whether hyperbaric oxygen (HBO) suppresses neuronal NADPH oxidase in a rat model of SAH.

Methods— Eighty-three Sprague-Dawley male rats were assigned to sham, SAH, and SAH treated with HBO groups. SAH was induced by endovascular perforation. HBO (2.8 atmospheres absolutes for 2 hours) was started at 1 hour after perforation. Rats were euthanized at 6 or 24 hours, and brains were collected for histology, biochemistry, and molecular biology studies including NADPH oxidase activity, gp91^phox mRNA expression, and lipid peroxidation assays. Mortality and neurological scores were evaluated.

Results— We observed an increased neuronal immunoreactivity of gp91^phox at 24 hours after SAH. The upregulation of gp91^phox mRNA was associated with increased oxidative stress. HBO decreased NADPH oxidase expression, activity, and the level of oxidative stress at 24 hours after SAH. HBO reduced neuronal injury and improved functional performance throughout the observation period.

Conclusion— HBO suppresses NADPH oxidase and oxidative stress in cerebral tissues at 24 hours after SAH.

Key Words: hyperbaric oxygenation • neuroprotection • oxidative stress • subarachnoid hemorrhage