Carbon monoxide used to protect mouse nerve cells from damage

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

The scientists, in a report published online Dec. 15 in Neurotoxicity Research, say that although carbon monoxide (CO) 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,” says lead author Sylvain Doré, Ph.D., an associate professor in the Department of Anesthesiology and Critical Care Medicine at Johns Hopkins University 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 cut-off in blood supply to nerve cells, but a good deal of the injury is also 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 (tPA) or other means, but these offer no protection from so-called “reperfusion” damage.

Doré and his team induced stroke in the mice by briefly blocking an artery to one side of the brain. Afterwards, the mice were exposed to either 125 parts-per-million (ppm) 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.

Doré 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,” says Doré.

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

Doré 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, M.D., of the Department of Anesthesiology and Critical Care at Johns Hopkins University School of Medicine also contributed to this story.


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