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目的：观察重复缺氧对小鼠在体脑乳酸含量以及Ｈ２Ｏ２对荷兰猪离体突触体乳酸含量的影响，并分析其作用机制。方法：采用酶氧化方法对突触体培养液中乳酸含量进行测定。结果：单次急性缺氧鼠脑内乳酸含量高，但在重复缺氧的作用下，鼠脑内乳酸的含量并未随缺氧时间的延长而增加。在突触体培养液中分别加入Ｈ２Ｏ２、ＦＣＣＰ、Ｒｏｔｅｎｏｎ，乳酸浓度比正常对照组显著性的增高。对突触体进行长时间Ｈ２Ｏ２处理，乳酸含量未见显著升高或降低。同时在突触体培养液中加入Ｈ２Ｏ２和ＦＣＣＰ，乳酸浓度相当于单独在突触体培养液分别加入Ｈ２Ｏ２与ＦＣＣＰ产生乳酸之和。结论：重复缺氧与Ｈ２Ｏ２处理可能激发脑与突触体内的抗自由基损伤防御系统；突触体从有氧呼吸到无氧酵解的转换主要不是由于Ｈ２Ｏ２对突触体膜的损伤。
OBJECTIVE: To observe the effects of repeated hypoxia on lactate content and Lactate content of isolated synaptosomes in guinea pigs in vivo and the mechanism of action. Methods: The content of lactic acid in synaptosomal culture fluid was determined by enzyme oxidation method. Results: The content of lactic acid in brain of single acute hypoxia rats was high, but the content of lactic acid in rat brain did not increase with the prolongation of hypoxia under the effect of repeated hypoxia. The concentrations of H2O2, FCCP, Rotenon and lactic acid in synaptosomal medium were significantly higher than those in normal control group. The synaptosome for long H2O2 treatment, lactic acid content was not significantly increased or decreased. Simultaneously, H 2 O 2 and FCCP were added to the synaptosomal medium. The concentration of lactate was equivalent to the sum of lactic acid produced by adding H2O2 and FCCP separately to the synaptosomal medium. CONCLUSIONS: Repeated hypoxia and H2O2 treatment may stimulate anti-free radical damage defense system in brain and synaptosomes. The conversion of synaptosomes from aerobic respiration to anaerobic glycolysis is not mainly due to the damage of synaptosomal membrane due to H2O2.