Carbon Monoxide Might Prevent Brain Damage Following Stroke

A new study shows that brain damage was reduced by as much as 62.2% in mice that inhaled low amounts of carbon monoxide (CO) after an induced stroke.

Researchers at Johns Hopkins University School of Medicine (Baltimore, MD, USA) induced stroke in mice by briefly blocking an artery to one side of the brain. Following the stroke, the mice were exposed to either 125 parts-per-million (ppm) or 250 ppm of CO; a control group was exposed to regular air. Each mouse was then tested for physical brain damage and function by observation of running patterns and reactions to certain stimuli. The results showed that the mice that were exposed only to air had brain damage of up to 49.9% of the side of the brain where ischemia was induced. In the mice that inhaled 125 ppm of CO immediately after stroke, brain damage dropped to 33.9%, and in the mice receiving 250 ppm, CO damage fell to 18.8%. Neurological function test scores were also significantly improved for mice that received CO after stroke. The results were similar for mice that were treated as long as one hour after stroke, and were significant even with mice that had been treated three hours after stroke. The researchers speculated that CO's protective effects might be due to its ability to dilate blood vessels, which increases blood flow, and to the gas's anti-inflammatory properties related to CO's capacity to reduce water in the brain. The study was published in the January 2009 issue of Neurotoxicity Research.

"CO is made naturally by the body and can serve a protective function under various circumstances,” said lead author Sylvain Doré, Ph.D., an associate professor in the department of anesthesiology and critical care medicine. "The idea for our experiment was to see if external CO could have a similar effect.”

A good deal of the injury caused during stroke is due to the release of tissue-damaging free radicals during reperfusion, when blood supply returns to the tissue after a period of ischemia. The absence of oxygen and nutrients from the blood during the ischemia creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress, rather than restoration of normal function.

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