Manukhina E B, Pokidyshev D A, Malyshev I Iu, Mashina S Iu, Viegant F, Mikoian V D, Kubrina L N, Vanin A F
Research Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow, Russia.
Izv Akad Nauk Ser Biol. 1998 Mar-Apr(2):300-4.
As was shown earlier, acute hypotensive shock induced by nitrogen oxide (NO) hyperproduction can be prevented by dosed adaptation to environmental factors. In this work we tested the hypothesis that the mechanism of this adaptive effect is based on limiting NO hyperproduction. It was shown that rat adaptation to stress completely prevented arterial depression and sharply increased revival rate of the animals after heat shock. Hypotension induced by heat shock was accompanied by almost 2.5-fold increase in NO production (EPR analysis) as compared to the control. At the background of preadaptation, heat shock did not increase NO production relative to the animals not subjected to heat shock. The data obtained agree with the proposal that the adaptation initiates NO-dependent mechanisms of limiting NO hyperproduction. Such limiting seems to be negatively regulated by NO.
如前所示，通过对环境因素进行剂量适应性调节可预防由一氧化氮（NO）过度产生所诱导的急性低血压休克。在本研究中，我们检验了这样一个假设，即这种适应性效应的机制基于限制NO的过度产生。结果表明，大鼠对应激的适应性完全预防了动脉血压降低，并显著提高了动物在热休克后的复苏率。与对照组相比，热休克诱导的低血压伴随着NO产生量几乎2.5倍的增加（电子顺磁共振分析）。在预先适应的背景下，与未遭受热休克的动物相比，热休克并未增加NO的产生量。所获得的数据与以下观点相符，即适应性启动了限制NO过度产生的NO依赖性机制。这种限制似乎受到NO的负调控。
