NDLI: Cilostazol, not aspirin, reduces ischemic brain injury via endothelial protection in spontaneously hypertensive rats.

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Cilostazol, not aspirin, reduces ischemic brain injury via endothelial protection in spontaneously hypertensive rats.

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Cilostazol, not aspirin, reduces ischemic brain injury via endothelial protection in spontaneously hypertensive rats.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sugiyama, Yukio Oyama, Naoki Kawamura, Miki Omura-Matsuoka, Emi Kitagawa, Kazuo Terasaki, Yasukazu Yagita, Yoshiki Sasaki, Tsutomu
Description	Country affiliation: Japan Author Affiliation: Oyama N ( Department of Neurology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. oyama@medone.med.osaka-u.ac.jp)
Abstract	BACKGROUND AND PURPOSE: It is well-established that hypertension leads to endothelial dysfunction in the cerebral artery. Recently, cilostazol has been used for the secondary prevention of ischemic stroke. Among antiplatelet drugs, phosphodiesterase inhibitors including cilostazol have been shown to have protective effects on endothelial cells. The aim of the present study is to investigate the effects of cilostazol and aspirin on endothelial nitric oxide synthase (eNOS) phosphorylation in the cerebral cortex, endothelial function, and infarct size after brain ischemia in spontaneously hypertensive rats (SHR). METHODS: Five-week-old male SHR received a 5-week regimen of chow containing 0.1% aspirin, 0.1% cilostazol, 0.3% cilostazol, or the vehicle control. The levels of total and Ser(1177)-phosphorylated eNOS protein in the cerebral cortex were evaluated by Western blot. To assess the contribution of eNOS in maintaining cerebral blood flow, we monitored cerebral blood flow by laser-Doppler flowmetry after L-N(5)-(1-iminoethyl)ornithine infusion. Additionally, we evaluated residual microperfusion using fluorescence-labeled serum protein and infarct size after transient focal brain ischemia. RESULTS: In SHR, the blood pressure and heart rate were similar among the groups. Cilostazol-treated SHR had a significantly higher ratio of phospho-eNOS/total eNOS protein than vehicle-treated and aspirin-treated SHR. Treating with cilostazol, but not aspirin, significantly improved cerebral blood flow response to L-N(5)-(1-iminoethyl)ornithine. Cilostazol also increased residual perfusion of the microcirculation and reduced brain damage after ischemia compared to vehicle control and aspirin. CONCLUSIONS: These findings indicate that cilostazol, but not aspirin, can attenuate ischemic brain injury by maintaining endothelial function in the cerebral cortex of SHR.
ISSN	00392499
e-ISSN	15244628
Journal	Stroke
Issue Number	9
Volume Number	42
Language	English
Publisher	Lippincott Williams & Wilkins (on behalf of the American Heart Association)
Publisher Date	2011-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Aspirin Pharmacology Brain Ischemia Endothelium, Vascular Physiopathology Fibrinolytic Agents Stroke Tetrazoles Animals Drug Therapy Cerebral Cortex Blood Supply Cerebrovascular Circulation Drug Effects Enzymology Nitric Oxide Synthase Type Iii Metabolism Phosphorylation Rats, Inbred Shr Research Support, Non-u.s. Gov't Discipline Cardiology
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine Neuroscience Advanced and Specialized Nursing Neurology (clinical)

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