Abstract
HMG-CoA reductase inhibitors (statins) are associated with improved stroke outcome. This observation has been attributed in part to the palliative effect of statins on cerebral hemodynamics and cerebral autoregulation (CA), which are mediated mainly through the upregulation of endothelium nitric oxide synthase (eNOS). Several animal studies indicate that statin pretreatment enhances cerebral blood flow after ischemic stroke, although this finding is not further supported in clinical settings. Cerebral vasomotor reactivity, however, is significantly improved after long-term statin administration in most patients with severe small vessel disease, aneurysmal subarachnoid hemorrhage, or impaired baseline CA.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Brain Ischemia / drug therapy
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Brain Ischemia / physiopathology
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Cerebral Small Vessel Diseases / drug therapy
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Cerebral Small Vessel Diseases / physiopathology
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Cerebrovascular Circulation / drug effects*
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Cerebrovascular Disorders / drug therapy
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Cerebrovascular Disorders / physiopathology
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Hemodynamics / drug effects*
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Humans
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Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology*
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Muscle Contraction / drug effects
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Muscle, Smooth, Vascular / drug effects
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Nitric Oxide Synthase Type III / metabolism
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Subarachnoid Hemorrhage / drug therapy
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Subarachnoid Hemorrhage / physiopathology
Substances
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Hydroxymethylglutaryl-CoA Reductase Inhibitors
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Nitric Oxide Synthase Type III