Martiashvili Z Sh, Azikuri G Sh, Zananian I I
Georgian Med News. 2006 Jul(136):87-90.
Though the mechanisms of hypoxic-ischemic preconditioning are under investigation, it is considered that nitric oxide can play a critical role in the formation of this phenomenon. Experiments on white rats for study of cerebral hemisphere masses were carried out on 22-nd day after 3-hours hypoxic-ischemic exposure: (a) on 7-day-old rats, (b) on 7-day-old rats but 30 minutes before this exposure animals 3-times underwent short lasting (5 minutes) hypoxic-ischemic impacts (preconditioning), (c) same as previous experimental condition, but 15 minutes before beginning of preconditioning, animals were intraperitoneally injected either by non selective nitric oxide synthase (NOS) inhibitor (L-NAME) or (d) inducible NO synthase (iNOS) selective inhibitor--aminoguanidine. Received results showed that 3-times preconditioning efficiently protect brain from three hours hypoxic-ischemic exposure. It is evident that nitric oxide play a critical role in this protection--it completely eliminated morphological manifestation of hypoxic-ischemic preconditioning while aminoguanidine--just partially decreased the volume of brain hypoxic-ischemic ischemic damage.
尽管缺氧缺血预处理的机制仍在研究中，但人们认为一氧化氮在这一现象的形成中可能起关键作用。在对大脑半球质量进行研究的实验中，对大白鼠在经历3小时缺氧缺血暴露后的第22天进行了如下实验：(a) 7日龄大鼠；(b) 7日龄大鼠，但在该暴露前30分钟，动物接受3次短暂（5分钟）的缺氧缺血冲击（预处理）；(c) 与先前实验条件相同，但在预处理开始前15分钟，给动物腹腔注射非选择性一氧化氮合酶（NOS）抑制剂（L-精氨酸甲酯）或(d) 诱导型一氧化氮合酶（iNOS）选择性抑制剂——氨基胍。所得结果表明，3次预处理能有效保护大脑免受3小时缺氧缺血暴露的影响。显然，一氧化氮在这种保护中起关键作用——它完全消除了缺氧缺血预处理的形态学表现，而氨基胍只是部分减少了脑缺氧缺血损伤的体积。
