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Ischemic and hemorrhagic strokes are the leading causes of disability in the United States. While considerable progress has been made in elucidating the etiology of these disorders, no therapies are available to prevent them. We have determined that heme oxygenase-1 (HO-1) plays a critical role in protecting against stroke. Importantly, HO-1 is expressed in the central nervous system (CNS) and is induced in response to ischemic stroke. We have also determined that HO-1 protects against the vasculature of the CNS during hemorrhagic stroke and that it can reduce the severity of experimental seizures in mice. Because these protective effects are associated with the production of carbon monoxide (CO), a gaseous byproduct of the action of HO-1, we investigated whether CO has neuroprotective effects on the CNS. We discovered that CO can protect against stroke in a time-dependent manner. CO administration also resulted in a decrease in brain infarction, indicating that the beneficial effects of CO are not dependent upon reperfusion. Additionally, CO is able to reduce the size of brain hemorrhages in two different mouse models of the disorder. In hemorrhagic stroke CO reduces brain edema and improves short and long term neurological outcome. As with ischemic stroke, the beneficial effects of CO in hemorrhagic stroke
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