SMALL DIFFERENCES IN INTRAISCHEMIC BRAIN TEMPERATURE CRITICALLY DETERMINE THE EXTENT OF ISCHEMIC NEURONAL INJURY
SMALL DIFFERENCES IN INTRAISCHEMIC BRAIN TEMPERATURE CRITICALLY DETERMINE THE EXTENT OF ISCHEMIC NEURONAL INJURY
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DOI：
10.1038/jcbfm.1987.127
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发表时间：
1987-12-01
影响因子：
6.3
通讯作者：
GINSBERG, MD
中科院分区：
文献类型：
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作者：
BUSTO, R;DIETRICH, WD;GINSBERG, MD
我们已经测试了脑温度的微小缺血内变化是否会影响短暂缺血的结果。为了测量脑温度，在四血管闭塞20分钟之前，将热电偶探针立体定位地放置到大鼠的左背外侧纹状体中。用加热灯将直肠温度保持在36 - 37 ℃，缺血前所有动物的纹状体温度为36 ℃。研究了六个动物亚组，包括缺血内纹状体脑温度未被调节或维持在33、34、36或39 ℃的大鼠。除了一组在再循环的第一个小时期间脑温度从36 ℃降低到33 ℃之外，将缺血后的脑温度调节在36 ℃。在缺血损伤结束时测量能量代谢产物，并在缺血后3天进行组织病理学评价。脑内缺血温度的变化对缺血结束时的能量代谢产物水平测量没有显著影响：在所有实验组中观察到类似程度的脑ATP、磷酸肌酸、葡萄糖和糖原的严重消耗和乳酸的升高。然而，缺血的组织病理学后果明显受到缺血内脑温度变化的影响。在海马体中，CA 1神经元在36 ℃时持续受损，但在34 ℃时没有。在背外侧纹状体内，缺血性细胞变化在36 ℃时出现在100%的半球中，但在34 ℃时仅出现在50%的半球中。在34 ℃的任何大鼠中均未观察到纹状体中央区内的缺血神经元，但在36 ℃的所有大鼠中均观察到。在纹状体温度不受控制的大鼠中，脑温从36 ℃降至30 - 31 ℃。C在缺血性损伤期间。在该组中，在纹状体区域内未观察到缺血性细胞变化，仅在CA 1海马区域内记录不一致。这些结果表明：（a）直肠温度不可靠地反映局部缺血期间的脑温度;（B）尽管在所有温度下局部缺血期间脑能量代谢物严重消耗，但局部缺血内脑温度的小增量显著加重了3天存活后的组织病理学变化;和（c）脑温度必须控制在33 ℃以上以确保一致的组织病理学结果。在局部缺血期间，脑温仅降低几度就具有显著的保护作用。
We have tested whether small intraischemic variations in brain temperature influence the outcome of transient ischemia. To measure brain temperature, a thermocouple probe was placed stereotaxically into the left dorsolateral striatum of rats prior to 20 min of four-vessel occlusion. Rectal temperature was maintained at 36-37.degree.C by a heating lamp, and striatal temperature prior to ischemia was 36.degree.C in all animals. Six animal subgroups were investigated, including rats whose intraischemic striatal brain temperature was not regulated, or was maintained at 33, 34, 36, or 39.degree.C. Postischemic brain temperature was regulated at 36.degree.C, except for one group in which brain temperature was lowered from 36.degree.C to 33.degree.C during the first hour of recirculation. Energy metabolites were measured at the end of the ischemic insult, and histopathological evaluation was carried out at 3 days after ischemia. Intraischemic variations in brain temperature had no significant influence on energy metabolite levels measure at the conclusion of ischemia: Severe depletion of brain ATP, phosphocreatine, glucose, and glycogen and elevation of lactate were observed to a similar degree in all experimental groups. The histopathological consequences of ischemia, however, were markedly influenced by variations in intraischemic brain temperature. In the hippocampus, CA1 neurons were consistently damaged at 36.degree.C, but not at 34.degree.C. Within the dorsolateral striatum, ischemic cell change was present in 100% of the hemispheres at 36.degree.C, but in only 50% at 34.degree.C. Ischemic neurons within the central zone of striatum were not observed in any rats at 34.degree.C, but in all rats at 36.degree.C. In rats whose striatal temperature was not controlled, brain temperature fell from 36 to 30-31.degree. C during the ischemic insult. In this group, no ischemic cell change was seen within striatal areas and was only inconsistently documented within the CA1 hippocampal region. These results demonstrate that (a) rectal temperature unreliably reflects brain temperature during ischemia; (b) despite severe depletion of brain energy metabolites during ischemia at all temperatures, small increments of intraischemic brain temperature markedly accentuate histopathological changes following 3-day survival; and (c) brain temperature must be controlled above 33.degree.C in order to ensure a consistent histopathological outcome. Lowering of the brain temperature by only a few degrees during ischemia confers a marked protective effect.