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Cerebral hypoperfusion was induced by three-vessel occlusion (3-VO) in rats, which subsequently received vehicle, ASA (6.34 mg\/kg), or clopidogrel (10 mg\/kg). Granulocyte colony-stimulating factor (G-CSF), which enhanced monocyte migration in an additional cell culture model, augmented cerebrovascular arteriogenesis in subgroups (40 \u03bcg\/kg). Cerebrovascular reactivity and vessel diameters were assessed at 7 and 21 days. Cerebrovascular reserve capacity was completely abolished after 3-VO and remained severely compromised after 7 (\u221214 \u00b1 14%) and 21 (\u22125 \u00b1 11%) days in the ASA groups in comparison with controls (4 \u00b1 5% and 10 \u00b1 10%) and clopidogrel (4 \u00b1 13% and 10 \u00b1 8%). It was still significantly decreased when ASA was combined with G-CSF (1 \u00b1 4%) compared with G-CSF alone (20 \u00b18%). Posterior cerebral artery diameters confirmed these data. Monocyte migration into the vessel wall, improved by G-CSF, was significantly reduced by ASA. Acetylsalicylic acid, but not clopidogrel, inhibits therapeutically augmented cerebral arteriogenesis.<\/jats:p>","DOI":"10.1038\/jcbfm.2011.113","type":"journal-article","created":{"date-parts":[[2011,8,10]],"date-time":"2011-08-10T04:06:06Z","timestamp":1312949166000},"page":"105-114","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":9,"title":["Acetylsalicylic Acid, but Not Clopidogrel, Inhibits Therapeutically Induced Cerebral Arteriogenesis in the Hypoperfused Rat Brain"],"prefix":"10.1177","volume":"32","author":[{"given":"Andr\u00e9","family":"Duelsner","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Cardiology and Angiology, Richard-Thoma-Laboratories for Arteriogenesis, Center for Cardiovascular Research and Experimental and Clinical Research Center, Charite' - Universitaetsmedizin Berlin, Berlin, 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