Thurman R G, Yuki T, Bleyman M A, Wendell G
Drug Alcohol Depend. 1979 Jan-Mar;4(1-2):119-29. doi: 10.1016/0376-8716(79)90052-8.
Simple models were developed to study changes in oxygen uptake in perfused rat liver and increases in ethanol metabolism in vivo. Results obtained 2.5 hours following a large dose of ethanol were quantitatively similar to those seen after 24 hours or 5 weeks. The rapidity of the increase indicated that SIAM represents an activation rather than an adaptation. Pathways responsible for the swift increase in alcohol metabolism (SIAM) in the perfused rat liver were investigated through the use of ouabain and were found to be related to diminished glycolysis and another unidentified pathway. Investigation of pathways responsible for the increase in ethanol metabolism in vivo following ethanol treatment implicated the alcohol dehydrogenase pathway as that mainly responsible for the adaptive increase, although a catalase-H2O2-dependent component was also involved. The rate of NADH reoxidation generally appeared to be the rate-limiting step. In addition, the genetic aspect of SIAM was indicated through selective breeding resulting in F1 generations of non-SIAM and SIAM rats.
构建了简单模型以研究灌注大鼠肝脏中氧摄取的变化以及体内乙醇代谢的增加。大剂量乙醇给药2.5小时后获得的结果在定量上与24小时或5周后观察到的结果相似。增加的快速性表明急性乙醇代谢增加（SIAM）代表一种激活而非适应。通过使用哇巴因研究了灌注大鼠肝脏中乙醇代谢快速增加（SIAM）的相关途径，发现其与糖酵解减少及另一条未明确的途径有关。对乙醇处理后体内乙醇代谢增加的相关途径进行研究表明，乙醇脱氢酶途径是适应性增加的主要原因，不过过氧化氢酶-H2O2依赖成分也参与其中。NADH再氧化速率通常似乎是限速步骤。此外，通过选择性育种产生非SIAM和SIAM大鼠的F1代，表明了SIAM的遗传方面。
