Dietrich W D, Busto R, Alonso O, Globus M Y, Ginsberg M D
Department of Neurology, University of Miami School of Medicine, FL 33101.
J Cereb Blood Flow Metab. 1993 Jul;13(4):541-9. doi: 10.1038/jcbfm.1993.71.
We investigated whether postischemic brain hypothermia (30 degrees C) would permanently protect the hippocampus following global forebrain ischemia. Global ischemia was produced in anesthetized rats by bilateral carotid artery occlusion plus hypotension (50 mm Hg). In the postischemic hypothermic group, brain temperature was maintained at 37 degrees C during the 10-min ischemic insult but reduced to 30 degrees C starting 3 min into the recirculation period and maintained at 30 degrees C for 3 h. In normothermic animals, intra- and postischemic brain temperature was maintained at 37 degrees C. After recovery for 3 days, 7 days, or 2 months, the extent of CA1 hippocampal histologic injury was quantitated. At 3 days after ischemia, postischemic hypothermia significantly protected the hippocampal CA1 sector compared with normothermic animals. For example, within the medial, middle, and lateral CA1 subsectors, the numbers of normal neurons were increased 20-, 13-, and 9-fold by postischemic hypothermia (p < 0.01). At 7 days after the ischemic insult, however, the degree of postischemic hypothermic protection was significantly reduced. In this case, the numbers of normal neurons were increased an average of only threefold compared with normothermia. Ultrastructural analysis of 7-day postischemic hypothermic rats demonstrated CA1 pyramidal neurons showing variable degrees of injury surrounded by reactive astrocytes and microglial cells. At 2 months after the ischemic insult, no trend for protection was demonstrated. In contrast to postischemic hypothermia, significant protection was seen at 2 months following intraischemic hypothermia. These data indicate that intraischemic, but not postischemic, brain hypothermia provides chronic protection to the hippocampus after transient brain ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
我们研究了缺血后脑低温（30摄氏度）是否能在全脑缺血后对海马体起到永久性保护作用。通过双侧颈动脉闭塞加低血压（50毫米汞柱）在麻醉大鼠中制造全脑缺血。在缺血后低温组中，在10分钟的缺血性损伤期间脑温维持在37摄氏度，但在再灌注期开始3分钟后降至30摄氏度，并在30摄氏度维持3小时。在常温动物中，缺血期间及缺血后脑温维持在37摄氏度。在恢复3天、7天或2个月后，对海马体CA1区的组织学损伤程度进行定量分析。缺血后3天，与常温动物相比，缺血后低温显著保护了海马体CA1区。例如，在内侧、中间和外侧CA1亚区，缺血后低温使正常神经元数量分别增加了20倍、13倍和9倍（p<0.01）。然而，在缺血性损伤7天后，缺血后低温保护程度显著降低。在这种情况下，与常温相比，正常神经元数量平均仅增加了三倍。对缺血后7天的低温大鼠进行超微结构分析显示，CA1锥体细胞显示出不同程度的损伤，周围有反应性星形胶质细胞和小胶质细胞。在缺血性损伤2个月后，未显示出保护趋势。与缺血后低温相反，缺血期间低温在2个月后显示出显著保护作用。这些数据表明，短暂性脑缺血后，缺血期间而非缺血后的脑低温能对海马体提供长期保护。（摘要截短至250字）
