Akopian N S, Sarkisian N V
Erevan State University.
Aviakosm Ekolog Med. 1996;30(1):36-42.
In normoxia, the orbitofrontal cortex and thalamic mediodorsal nucleus (MDN) basically inhibit the pulse activity of bulbar respiratory neurons and respiration in general. During initial hypoxia (4,000-5,000 m) a slight reduction of PO2 in the inspired air increases excitability of all the brain structures including those under study. However, strengthening of the orbitofrontal cortex and MDN inhibitory effect was leveled down by activizing brain structures, and the direct exciting effect of reduced PO2 on peripheral and central chemoreceptors. As a result, respiration became hurried in that period. Still, this inhibitory effect appears to play a positive role too. Unobstructed enhancement of activizing neural and humoral regulators of respiration might have led to intense hyperventilation fraught with an opposite action, i.e., inhibition, if not arrest of respiration consequent to reduced PO2 blood level, etc. Under acute hypoxia (7.5,000-8,000 m), oxygen deficit brings about inhibition, of all the brain structures including the orbitofrontal cortex and MDN. Moderation of their inhibitory effect in this period also plays an important role as it stimulates liberation of activizing systems and a relative increase in the ventilatory function of respiration.
在正常氧分压情况下，眶额皮质和丘脑背内侧核（MDN）基本上抑制延髓呼吸神经元的脉冲活动及整体呼吸。在初期缺氧（海拔4000 - 5000米）时，吸入空气中PO2的轻微降低会增加包括所研究结构在内的所有脑结构的兴奋性。然而，通过激活脑结构以及降低的PO2对外周和中枢化学感受器的直接兴奋作用，眶额皮质和MDN的抑制作用增强得以减弱。结果，在那个阶段呼吸变得急促。不过，这种抑制作用似乎也发挥着积极作用。如果呼吸的激活神经和体液调节因子不受阻碍地增强，可能会导致强烈的过度通气，若因血液中PO2水平降低等情况，这种过度通气可能会产生相反的作用，即抑制甚至停止呼吸。在急性缺氧（海拔7500 - 8000米）时，氧亏会导致包括眶额皮质和MDN在内的所有脑结构受到抑制。在这个阶段减弱它们的抑制作用也起着重要作用，因为它刺激激活系统的释放，并使呼吸的通气功能相对增加。
