作者: Zoltán Süle , Éva Mracskó , Erika Bereczki , Miklós Sántha , Tamás Csont
DOI: 10.1016/J.LFS.2009.04.011
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摘要: Abstract Aims: Apolipoprotein B-100 (apoB-100) has been implicated in hyperlipidemia, which contributes to the pathogenesis of vascular disorders. Our aim was investigate whether expression human apoB-100 transgenic mice and/or a high-cholesterol diet cause cerebral microvascular lesions, and these conditions augment ischemia-related capillary damage. Main methods: Human overexpressing (Tg( ), n = 23) wild-type (C5/B6, Wt, = 26) were supplied with standard or 2% cholesterol-enriched for 17–19 weeks. Cerebral ischemia induced by unilateral common carotid artery occlusion. Cortical samples embedded electron microscopy. Microvascular density (number profiles/examined area), lumen diameter, swelling astrocytic endfeet, occurrence endothelial microvilli (affected capillaries expressed as ratio all encountered), intact (devoid above pathology) calculated. Key findings: The coincided decreased cortical (195 ± 7 vs. 223 ± 8 vessels/mm 2 , Wt; P Significance: overexpression alters network diameter capillaries, may compromise cerebrovascular reactivity during ischemia.