Acetylsalicylic acid, but not clopidogrel, inhibits therapeutically induced cerebral arteriogenesis in the hypoperfused rat brain

作者：Duelsner Andre^*; Gatzke Nora; Glaser Johanna; Hillmeister Philipp; Li Meijing; Lee Eun Ji; Lehmann Kerstin; Urban Daniel; Meyborg Heike; Stawowy Philipp; Busjahn Andreas; Nagorka Stephanie; Persson Anja Bondke; Buschmann Ivo R

来源：Journal of Cerebral Blood Flow and Metabolism, 2012, 32(1): 105-114.

DOI：10.1038/jcbfm.2011.113

• arteriogenesis
• brain ischemia
• cerebral blood flow
• cerebrovascular disease
• platelet inhibitors
• macrophages

This study investigated the effects of acetylsalicylic acid (ASA) and clopidogrel, standardly used in the secondary prevention of vascular occlusions, on cerebral arteriogenesis in vivo and in vitro. Cerebral hypoperfusion was induced by three-vessel occlusion (3-VO) in rats, which subsequently received vehicle, ASA (6.34mg/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 mu g/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 (-14 +/- 14%) and 21 (-5 +/- 11%) days in the ASA groups in comparison with controls (4 +/- 5% and 10 +/- 10%) and clopidogrel (4 +/- 13% and 10 +/- 8%). It was still significantly decreased when ASA was combined with G-CSF (1 +/- 4%) compared with G-CSF alone (20 +/- 8%). 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. Journal of Cerebral Blood Flow & Metabolism (2012) 32, 105-114; doi:10.1038/jcbfm.2011.113; published online 10 August 2011

• 出版日期2012-1