MAGNETIC-RESONANCE-IMAGING OF BRAIN EDEMA IN THE NEONATAL RAT - A COMPARISON OF SHORT AND LONG-TERM HYPOXIA-ISCHEMIA
MAGNETIC-RESONANCE-IMAGING OF BRAIN EDEMA IN THE NEONATAL RAT - A COMPARISON OF SHORT AND LONG-TERM HYPOXIA-ISCHEMIA
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DOI：
10.1203/00006450-199507000-00020
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发表时间：
1995-07-01
影响因子：
3.6
通讯作者：
MARTIN, E
中科院分区：
文献类型：
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作者：
RUMPEL, H;BUCHLI, R;MARTIN, E
采用弥散加权和横向弛豫时间（T-2）加权磁共振成像研究缺氧缺血时间[单侧颈总动脉（CCA）结扎和暴露于8%氧气]与7天龄大鼠脑水肿的体内可视化之间的关系。CCA结扎后，将35只动物按暴露于8%氧气的时间长短分为5组：无暴露组（n = 9）、15 min组（n = 12）、30 min组（n = 5）和1 h组（n = 9）; 6只动物作为对照组。在缺氧缺血后2 h获取弥散加权成像，连续记录7 d的T-2加权成像，并在21 d时通过组织学检查记录结果。在长时间缺氧缺血性损伤（30分钟或更长时间）恢复的所有动物中，同侧皮质中水的表观扩散系数显著降低，而在暴露于15分钟缺氧的动物中，只有40%的动物出现这种情况。脑组织T-2延长仅在前一组。这些结果表明，短暂的和可逆的改变生理水隔短期缺氧缺血，但不可逆的水肿形成长期缺氧缺血。他们支持这样的假设，即缺氧缺血的持续时间决定了血管源性水肿和梗死是否在最初的细胞毒性水肿之后。
Diffusion-weighted and transversal relaxation time (T-2)-weighted magnetic resonance imaging were used to study the relationship between the duration of hypoxia-ischemia [unilateral common carotid artery (CCA) ligation and exposure to 8% oxygen] and the in vivo visualization of brain edema in 7-d-old rats. After CCA ligation, 35 animals were divided into five groups according to the length of exposure to 8% oxygen: no exposure (n = 9), 15 min (n = 12), 30 min (n = 5), and 1 h (n = 9) exposure; six animals served as controls. Diffusion weighted images were acquired 2 h after the hypoxic-ischemic insult, sequential T-2 weighted images were recorded for up to 7 d and the outcome was documented by histologic examination at 21 d. The apparent diffusion coefficient of water in the ipsilateral cortex was significantly decreased in all animals recovering from prolonged hypoxic-ischemic insult (30 min and longer), whereas this was the case in only 40% of animals exposed to 15 min of hypoxia. Moreover, T-2 prolongation of brain tissue occurred only in the former group. These results indicate transient and reversible alterations of physiologic water compartmentation for short term hypoxia-ischemia, but irreversible edema formation for long term hypoxia-ischemia. They support the hypothesis that the duration of hypoxia-ischemia determines whether a vasogenic edema and infarction follows the initial cytotoxic edema.