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Published Online
on March 23, 2006

Stroke. 2006
Published online before print March 23, 2006, doi: 10.1161/01.STR.0000217310.88450.c3
A more recent version of this article appeared on May 1, 2006
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Submitted on September 29, 2005
Revised on December 8, 2005
Accepted on February 3, 2006

Hyperbaric Oxygen Suppresses NADPH Oxidase in a Rat Subarachnoid Hemorrhage Model

Robert P. Ostrowski MD, PhD; Jiping Tang MD; and John H. Zhang MD, PhD*

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.

* To whom correspondence should be addressed. 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, gp91phox mRNA expression, and lipid peroxidation assays. Mortality and neurological scores were evaluated.

Results--We observed an increased neuronal immunoreactivity of gp91phox at 24 hours after SAH. The upregulation of gp91phox 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