Erythropoietin and cerebral vascular protection: role of nitric oxide.
Cerebral vasospasm after subarachnoid hemorrhage (SAH) is a major clinical problem causing cerebral ischemia and infarction. The pathogenesis of vasospasm is related to a number of pathological processes including endothelial damage and alterations in vasomotor function leading to narrowing of arterial diameter and a subsequent decrease in cerebral blood flow. Discovery of the tissue protective effects of erythropoietin (EPO) stimulated the search for therapeutic application of EPO for the prevention and treatment of cerebrovascular disease. Recent studies have identified the role of EPO in vascular protection mediated by the preservation of endothelial cell integrity and stimulation of angiogenesis. In this review, we discuss the EPO-induced activation of endothelial nitric oxide (NO) synthase and its contribution to the prevention of cerebral vasospasm.
Santhanam
Anantha Vijay R
AV
Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.
Katusic
Zvonimir S
ZS
D000818:Animals; D002536:Cerebral Arteries / Q000201:enzymology*; D004921:Erythropoietin / Q000494:pharmacology* / Q000502:physiology*; D006801:Humans; D053614:Janus Kinase 2 / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000502:physiology*; D010766:Phosphorylation; D011485:Protein Binding; D017467:Receptors, Erythropoietin / Q000378:metabolism; D011994:Recombinant Proteins; D020301:Vasospasm, Intracranial / Q000378:metabolism*
D017467:Receptors, Erythropoietin; D011994:Recombinant Proteins; D004921:Erythropoietin; D052250:Nitric Oxide Synthase Type III; C507924:JAK2 protein, human; D053614:Janus Kinase 2