International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
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Int. J. Dev. Neurosci. · Feb 2006
Caffeic acid phenethyl ester (CAPE) attenuates cerebral vasospasm after experimental subarachnoidal haemorrhage by increasing brain nitric oxide levels.
Cerebral vasospasm, a medical complication of aneurysmal subarachnoid hemorrhage (SAH), is associated with high morbidity and mortality rates, even after the aneurysm has been secured surgically or endovascularly. Evidence accumulated during the last decade suggest that scavenging a vasodilator, nitric oxide (NO), by superoxide anions (O(2)(-)), and activating a strong vasoconstructor, protein kinase C (PKC), are the two most important mechanisms in the pathogenesis of vasospasm. Our aim in this study was to determine whether caffeic acid phenethyl ester (CAPE), a non-toxic oxygen free radical scavenger, prevents vasospasm in an experimental rat model of SAH. ⋯ Our results indicate that CAPE is effective in attenuating delayed cerebral vasoconstriction following experimental SAH. Our findings also suggest that the elevation of lipid peroxidation and reduction of NO bioavailability, resulting from the generation and the interaction of free radicals, have a significant role in the pathogenesis of vasospasm after SAH.