Bertrand N, Ishii H, Spatz M
Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Neurosci Lett. 1992 Dec 14;148(1-2):81-4. doi: 10.1016/0304-3940(92)90809-l.
Temporal ischemic changes in glycerol and energy metabolites were studied in the striatum, hippocampus and cortex of gerbils subjected to 15 min of bilateral carotid artery occlusion alone or with various periods of recirculation. The same tissue sample served for the determination of glycerol and energy reserve by a simple enzymatic fluoro- and spectrometric assay after perchloric acid extraction. Cerebral ischemia increased the levels of glycerol (8- to 10-fold) and depleted the energy stores. During the first hour of recirculation, the glycerol content decreased and thereafter (at 2 h), normalized in all structures. However, the glycerol content was still twice as high in the striatum and hippocampus as compared to their respective controls. At the same time, an incomplete restoration of energy reserves was observed in these structures. The findings indicate that glycerol is not a stable postischemic indicator of the ischemia-induced membrane damage.
在单独进行15分钟双侧颈动脉闭塞或伴有不同再灌注时间的沙土鼠的纹状体、海马体和皮质中，研究了甘油和能量代谢物的短暂缺血变化。通过高氯酸提取后，用简单的酶促荧光和光谱测定法对同一组织样本进行甘油和能量储备的测定。脑缺血增加了甘油水平（8至10倍）并耗尽了能量储备。在再灌注的第一个小时内，甘油含量下降，此后（2小时时），所有结构中的甘油含量恢复正常。然而，纹状体和海马体中的甘油含量仍比各自的对照组高两倍。与此同时，在这些结构中观察到能量储备的不完全恢复。这些发现表明，甘油不是缺血诱导的膜损伤的稳定的缺血后指标。
