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(Stroke. 2008;39:1548.)
© 2008 American Heart Association, Inc.

Original Contributions

Mild Induced Hypertension Improves Blood Flow and Oxygen Metabolism in Transient Focal Cerebral Ischemia

Hwa Kyoung Shin, PhD; Masaki Nishimura, MD; Phillip B. Jones, PhD; Hakan Ay, MD; David A. Boas, PhD; Michael A. Moskowitz, MD Cenk Ayata, MD

From the Stroke and Neurovascular Regulation Laboratory (H.K.S., M.N., M.A.M., C.A.) and the Martinos Center for Biomedical Imaging (P.B.J., H.A., D.A.B.), Department of Radiology, and the Stroke Service and Neuroscience Intensive Care Unit, Department of Neurology (C.A.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Mass.

Correspondence to Cenk Ayata, MD, Stroke and Neurovascular Regulation Laboratory, 149 13th Street, Room 6403, Charlestown, MA 02129. E-mail cayata{at}partners.org

Background and Purpose— In focal ischemic cortex, cerebral blood flow autoregulation is impaired, and perfusion passively follows blood pressure variations. Although it is generally agreed that profound hypotension is harmful in acute stroke, the hemodynamic and metabolic impact of increased blood pressure on the ischemic core and penumbra are less well understood. We, therefore, tested whether pharmacologically induced hypertension improves cerebral blood flow and metabolism and tissue outcome in acute stroke using optical imaging with high spatiotemporal resolution.

Methods— Cerebral blood flow, oxyhemoglobin, and cerebral metabolic rate of oxygen were measured noninvasively using simultaneous multispectral reflectance imaging and laser speckle flowmetry during distal middle cerebral artery occlusion in mice. Hypertension was induced by phenylephrine infusion starting 10 or 60 minutes after ischemia to raise blood pressure by 30% for the duration of ischemia; control groups received saline infusion.

Results— Mild induced hypertension rapidly increased cerebral blood flow, oxyhemoglobin, and cerebral metabolic rate of oxygen in both the core and penumbra and prevented the expansion of cerebral blood flow deficit during 1 hour distal middle cerebral artery occlusion. Induced hypertension also diminished the deleterious effects of periinfarct depolarizations on cerebral blood flow, oxyhemoglobin, and cerebral metabolic rate of oxygen without altering their frequency. Consistent with this, mild induced hypertension reduced infarct volume by 48% without exacerbating tissue swelling when measured 2 days after 1 hour transient distal middle cerebral artery occlusion.

Conclusions— Our data suggest that mild induced hypertension increases collateral cerebral blood flow and oxygenation and improves cerebral metabolic rate of oxygen in the core and penumbra, supporting its use as bridging therapy in acute ischemic stroke until arterial recanalization is achieved.

Key Words: cerebral metabolic rate of oxygen • laser speckle flowmetry • middle cerebral artery occlusion • multispectral reflectance imaging • stroke

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