Background: Risks related to rebleeding of a ruptured intracranial aneurysm have decreased. However, ischemic neurologic deficits related to vasospasm are still the leading causes of mortality ami morbidity. It is well known that vasospasm is a dynamic process affected by various factors. The severity of vasospasm in animal models and clinical observations differ from each other. This variability has not been completely explained by blood and blood degradation products. Therefore, metabolites released from the damaged vessel wall during the bleeding are thought to play an important role in vasospasm.