Supplemental

Klaus-Dieter E. Pawlik
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引用次数: 116

Abstract

Materials and Methods Animal models of cerebral hypoperfusion and therapeutic induction of collateral growth For evalution of the effects of G-CSF on cerebral arteriogenesis, two different models of cerebral hypoperfusion were used, three vessel occlusion (3-VO) in rats [1,2] and left common carotid artery occlusion (CCAO) in mice (Fig. 1A). 3-VO includes bilateral vertebral artery occlusion followed by ligation of the left common carotid artery as described previously [1,3]. To show relevance of 3-VO in rats and CCAO in mice for the induction of permanent hypoperfusion, CCAO was performed in an additional rat group (n = 6) and compared with 3-VO. Cerebral blood flow was measured by laser Doppler flowmetry. Anaesthesia was initiated with 50 mg/kg ketamine/4 mg/kg xylazine i.p. in rats and 100 mg/kg ketamine/10 mg/kg xylazine i.p. in mice and maintained with 1-2% isoflurane in oxygen p.i.. In all groups Ropivacaine (5 mg/kg; Naropin®, AstraZeneca) was infiltrated into the wounds against pain.
补充
为了评估G-CSF对脑动脉发生的影响,我们使用了两种不同的脑灌注不足模型,大鼠三支血管闭塞(3-VO)[1,2]和小鼠左颈总动脉闭塞(CCAO)(图1A)。3- vo包括双侧椎动脉闭塞,然后如前所述结扎左侧颈总动脉[1,3]。为了显示大鼠3-VO和小鼠CCAO在诱导永久性灌注不足中的相关性,我们在另一组大鼠(n = 6)中进行CCAO,并与3-VO进行比较。采用激光多普勒血流仪测量脑血流。麻醉开始时,大鼠注射50mg /kg氯胺酮/ 4mg /kg噻嗪,小鼠注射100mg /kg氯胺酮/ 10mg /kg噻嗪,并用1-2%异氟烷供氧。各组罗哌卡因(5 mg/kg;纳洛平®,阿斯利康)渗透到伤口止痛。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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