Piérard C, Champagnat J, Denavit-Saubie M, Gillet B, Beloeil J C, Guezennec C Y, Barrère B, Pérès M
Institut de Médecine Aérospatiale, Base d'Essais de Brétigny, Bretigny-sur-Orge, France.
Neuroreport. 1995 Dec 29;7(1):281-5.
Mammals react to acute hypoxia with an initial augmentation and a secondary depression of the respiratory rhythm generated by brain stem neuronal networks. To investigate the cytosolic level of energy rich phosphorus metabolites during these responses, we developed 31P nuclear magnetic resonance spectroscopy of the brain stem. Moderate hypoxia (paO2 = 40 mmHg, 2 min) caused a reversible 62 +/- 15% respiratory rhythm depression and decreased cytosolic phosphocreatine levels by 43 +/- 11% (p < 0.01, n = 7) without affecting adenosine triphosphate levels. Cellular metabolic depletion therefore contributes to the brain stem response to hypoxia, and appears to reflect adaptive mechanisms to limited oxygen availability in the brain stem.
哺乳动物对急性缺氧的反应是，脑干神经网络产生的呼吸节律先增强，随后减弱。为了研究这些反应过程中富含能量的磷代谢物的胞质水平，我们开发了脑干的31P核磁共振波谱技术。中度缺氧（动脉血氧分压 = 40 mmHg，持续2分钟）导致呼吸节律可逆性降低62±15%，胞质磷酸肌酸水平降低43±11%（p<0.01，n = 7），而三磷酸腺苷水平不受影响。因此，细胞代谢耗竭是脑干对缺氧反应的原因，并且似乎反映了脑干对有限氧供应的适应性机制。
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