Johns Hopkins Gazette | December 15, 2008
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The newspaper of The Johns Hopkins University December 15, 2008 | Vol. 38 No. 15
'Toxic' Carbon Monoxide May Prevent Brain Damage After Stroke

By Eric Vohr
Johns Hopkins Medicine

Researchers at Johns Hopkins have shown that brain damage was reduced by as much as 62.2 percent in mice who inhaled low amounts of carbon monoxide, or CO, after an induced stroke.

The scientists, in a report published online today, Dec. 15, in Neurotoxicity Research, say that although carbon monoxide gas has a long reputation as an odorless, colorless cause of organ damage and even death, there is now evidence that it can protect nerve cells from damage.

"CO is made naturally by the body and can serve a protective function under various circumstances," said lead author Sylvain Dore (doh-ray), an associate professor in the Department of Anesthesiology and Critical Care Medicine at the School of Medicine. "The idea for our experiment was to see if external CO could have a similar effect."

Some of the brain damage associated with stroke results directly from a cutoff in blood supply to nerve cells, but a good deal of the injury is due to chemical reactions and the resulting release of tissue-damaging free radicals when blood flow is restored. Currently the only treatment for such strokes is to clear out the blood clot with clot busters, such as tissue plasminogen activator or other means, but these offer no protection from so-called "reperfusion" damage.

Dore and his team induced stroke in the mice by briefly blocking an artery to one side of the brain. Afterward, the mice were exposed to either 125 parts-per-million or 250 ppm of CO. A control group was exposed only to air. Each was tested for physical brain damage and function, mainly by observing running patterns and reactions to certain stimuli.

Results showed that mice exposed only to air had brain damage to 49.9 percent of the side of the brain where the blood supply was cut off. In mice that inhaled 125 ppm of CO immediately after stroke, brain damage dropped to 33.9 percent, and in mice getting 250 ppm, CO damage fell to 18.8 percent. Neurological function test scores were also significantly improved for mice that received CO after stroke.

Dore and his team say the results were almost the same for mice who were treated as long as one hour after stroke, and results even looked good with mice treated three hours after stroke.

"It is important that we still see CO's neuroprotection at one and three hours since many stroke victims will not receive immediate treatment," Dore said.

Dore and his team speculate that CO's protective effects might be due to its ability to dilate or open blood vessels, therefore increasing blood flow; its anti-inflammatory properties, preventing cell death caused by inflammation; and its capacity to reduce water in the brain. Excessive water in the brain increases intracranial pressure, which kills brain cells.

Dore says future research will focus on finding the lowest possible effective therapeutic dose of CO that protects against stroke damage in order to limit CO toxicity that is known to occur at higher doses.

Roughly 700,000 people experience a stroke in the United States annually. Of those, 87 percent suffer ischemic stroke, which is caused by a blocked artery in the brain.

Emil Zeynalov, of the Department of Anesthesiology and Critical Care Medicine at the School of Medicine, also contributed to this research.

This research was supported by the National Institutes of Health.


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