Go K G, Prenen G H, Korf J
Department of Neurosurgery, University of Groningen, The Netherlands.
Metab Brain Dis. 1988 Dec;3(4):257-63. doi: 10.1007/BF00999535.
This study was designed to determine the effect of fasting upon cerebral hypoxic-ischemic injury. In the first part of the study the effect of fasting was determined for survival, brain tissue water and kation contents, and blood-brain barrier integrity. In the second part of the study the administration of the substrates beta-hydroxybutyrate (BHB) and glucose has been evaluated regarding their influence upon the effect of fasting. The study used the Levine-Klein model of unilateral carotid occlusion and hypoxia because it mimics clinical situations of ischemia with hypoxia. The data show that fasting did protect rats from developing brain infarction following hypoxia-ischemia. Hypoglycemia seems to be involved in the mitigation of ischemic blood-brain barrier disruption. The plasma glucose level seems to be not the only factor involved in the genesis of the tissue kation changes. Starvation-induced ketosis probably does not play a role in the protection mechanism.
本研究旨在确定禁食对脑缺氧缺血性损伤的影响。在研究的第一部分,测定了禁食对存活率、脑组织水分和阳离子含量以及血脑屏障完整性的影响。在研究的第二部分,评估了底物β-羟基丁酸酯(BHB)和葡萄糖的给药对禁食效果的影响。该研究使用了单侧颈动脉闭塞和缺氧的Levine-Klein模型,因为它模拟了伴有缺氧的缺血临床情况。数据表明,禁食确实能保护大鼠在缺氧缺血后不发生脑梗死。低血糖似乎参与了缺血性血脑屏障破坏的减轻过程。血浆葡萄糖水平似乎不是组织阳离子变化发生的唯一因素。饥饿诱导的酮症可能在保护机制中不起作用。