Klemm W R
J Neurosci Res. 1978;3(5-6):353-8. doi: 10.1002/jnr.490030506.
Previous research with two biochemical markers of acute ethanol damage (sialic acid and 2-deoxyribose) raised the possibility that tolerance developed by chronic ingestion of ethanol could protect brain cells from "damaging" effects of large, acute doses of ethanol. However, this hypothesis required demonstration that chronic consumption was not damaging. This issue was investigated histologically in adult rats that voluntarily consumed massive doses of ethanol daily (range of 11 to 18 gm/kg/rat/day) for 28 days. By all indices (thickness measures of neocortex, hippocampus, and cerebellar molecular layer; and specific cell counts of neocortex and cerebellum), none of the ethanol-exposed rats, even those with intentional nutritional deficiencies, revealed any physical sign of damage compared to control rats.
先前针对急性乙醇损伤的两种生化标志物（唾液酸和2-脱氧核糖）开展的研究提出了这样一种可能性，即长期摄入乙醇所产生的耐受性能够保护脑细胞免受大剂量急性乙醇的“损伤”作用。然而，这一假说需要证明长期饮酒不会造成损害。在成年大鼠身上通过组织学方法对这一问题进行了研究，这些成年大鼠每天自愿摄入大剂量乙醇（每只大鼠每天11至18克/千克），持续28天。通过所有指标（新皮层、海马体和小脑分子层的厚度测量；以及新皮层和小脑的特定细胞计数），与对照大鼠相比，所有接触乙醇的大鼠，即使是那些故意存在营养缺乏的大鼠，均未显示出任何损伤的体征。
