Gozal D
Department of Pediatrics, Tulane University School of Medicine, New Orleans, Louisiana 70112, USA.
J Appl Physiol (1985). 1998 Jul;85(1):129-32. doi: 10.1152/jappl.1998.85.1.129.
In humans, the hypoxic ventilatory response (HVR) is augmented when preceded by a short hyperoxic exposure (Y. Honda, H. Tani, A. Masuda, T. Kobayashi, T. Nishino, H. Kimura, S. Masuyama, and T. Kuriyama. J. Appl. Physiol. 81: 1627-1632, 1996). To examine whether neuronal nitric oxide synthase (nNOS) is involved in such hyperoxia-induced HVR potentiation, 17 male Sprague-Dawley adult rats underwent hypoxic challenges (10% O2-5% CO2-balance N2) preceded either by 10 min of room air (-O2) or of 100% O2 (+O2). At least 48 h later, similar challenges were performed after the animals received the selective nNOS inhibitor 7-nitroindazole (25 mg/kg ip). In -O2 runs, minute ventilation (VE) increased from 121.3 +/- 20.5 (SD) ml/min in room air to 191.7 +/- 23.8 ml/min in hypoxia (P < 0.01). After +O2, VE increased from 114.1 +/- 19.8 ml/min in room air to 218.4 +/- 47. 0 ml/min in hypoxia (+O2 vs. -O2: P < 0.005, ANOVA). After 7-nitroindazole administration, HVR was not affected in the -O2 treatment group with VE increasing from 113.7 +/- 17.8 ml/min in room air to 185.8 +/- 35.0 ml/min in hypoxia (P < 0.01). However, HVR potentiation in +O2-exposed animals was abolished (111.8 +/- 18. 0 ml/min in room air to 184.1 +/- 35.6 ml/min in hypoxia; +O2 vs. -O2: P not significant). We conclude that in the conscious rat nNOS activation mediates essential components of the HVR potentiation elicited by a previous short hyperoxic exposure.
在人类中，短暂的高氧暴露后，低氧通气反应（HVR）会增强（Y. 本田、H. 谷、A. 增田、T. 小林、T. 西野、H. 木村、S. 益山和T. 栗山。《应用生理学杂志》81: 1627 - 1632, 1996）。为了研究神经元型一氧化氮合酶（nNOS）是否参与这种高氧诱导的HVR增强，对17只成年雄性Sprague - Dawley大鼠进行低氧挑战（10% O₂ - 5% CO₂ - 其余为N₂），挑战前分别给予10分钟的室内空气（-O₂）或100% O₂（+O₂）。至少48小时后，在动物接受选择性nNOS抑制剂7 - 硝基吲唑（25 mg/kg腹腔注射）后，进行类似的挑战。在 -O₂组实验中，分钟通气量（VE）从室内空气中的121.3±20.5（标准差）ml/min增加到低氧时的191.7±23.8 ml/min（P < 0.01）。在 +O₂组中，VE从室内空气中的114.1±19.8 ml/min增加到低氧时的218.4±47.0 ml/min（+O₂组与 -O₂组比较：P < 0.005，方差分析）。给予7 - 硝基吲唑后，-O₂治疗组的HVR未受影响，VE从室内空气中的113.7±17.8 ml/min增加到低氧时的185.8±35.0 ml/min（P < 0.01）。然而，+O₂暴露动物的HVR增强被消除（室内空气中为111.8±18.0 ml/min，低氧时为184.1±35.6 ml/min；+O₂组与 -O₂组比较：P无显著性差异）。我们得出结论，在清醒大鼠中，nNOS激活介导了先前短暂高氧暴露引起的HVR增强的关键成分。
