Cragg P A, Drysdale D B, Hamilton J H
J Physiol. 1986 Jan;370:489-99. doi: 10.1113/jphysiol.1986.sp015946.
The cause of the initial hyperventilation, which occurs on exposure to O2 at high pressure (o.h.p.), has been investigated by measuring tidal volume (VT), frequency of breathing (f) and hence ventilation (VE) in thirty-six barbiturate-anaesthetized rats, with or without their glossopharyngeal (IX) nerves sectioned, during 30-60 min of exposure to o.h.p. at 4, 6 or 8 atm absolute. In intact rats the rates of rise of VT, f and VE with time during exposure to o.h.p. were smallest at 4 and greatest at 8 atm absolute. In IX-sectioned rats the rates of rise of VT at 4, 6 and 8 atm absolute and of f at 4 atm absolute were similar to those of intact rats. At 6 atm absolute and even more so at 8 atm absolute, however, f decreased. Hence the slope of VE in IX-sectioned compared with intact rats was similar at 4 atm absolute but smaller at 6 and 8 atm absolute. In fact at 8 atm absolute VE remained constant in IX-sectioned rats. Since the slope of VE versus time in intact rats was steeper the greater the pressure and since the removal of carotid bodies in IX-sectioned rats reduced the VE slope at 6 and 8 atm absolute, the stimulus to the hyperventilation induced by o.h.p. cannot be an accumulation of CO2 in the brain resulting from the lack of O2 desaturation of haemoglobin. This theory would predict that VE should be identical at all pressures above 3.5 atm absolute. The findings in the IX-sectioned rats indicate a major contribution of the carotid bodies to the f increase in o.h.p. They may be stimulated by a histotoxic hypoxia induced by early O2 poisoning. Since the VT increase on exposure to o.h.p. was both large and fairly similar in intact and IX-sectioned rats, it is suggested that a large part of the VT increase was caused by stimulation of the central chemoreceptors by lactic acidosis induced by an o.h.p.-induced histotoxic hypoxia of the brain.
通过测量三十六只巴比妥麻醉大鼠在绝对压力为4、6或8个大气压下暴露于高压氧（o.h.p.）30 - 60分钟期间的潮气量（VT）、呼吸频率（f）以及通气量（VE），研究了在暴露于高压氧时最初出现的过度通气的原因，这些大鼠有的切断了舌咽（IX）神经，有的未切断。在完整大鼠中，暴露于高压氧期间，VT、f和VE随时间的上升速率在绝对压力为4时最小，在绝对压力为8时最大。在切断IX神经的大鼠中，绝对压力为4、6和8时VT的上升速率以及绝对压力为4时f的上升速率与完整大鼠相似。然而，在绝对压力为6时，尤其是在绝对压力为8时，f下降。因此，与完整大鼠相比，切断IX神经的大鼠在绝对压力为4时VE的斜率相似，但在绝对压力为6和8时较小。实际上，在绝对压力为8时，切断IX神经的大鼠的VE保持恒定。由于完整大鼠中VE与时间的斜率随压力升高而更陡，并且由于切断IX神经的大鼠中颈动脉体的切除降低了绝对压力为6和8时的VE斜率，所以高压氧诱导的过度通气的刺激因素不可能是由于血红蛋白缺乏氧去饱和导致大脑中二氧化碳的积累。该理论预测在绝对压力高于3.5个大气压时，VE在所有压力下都应相同。切断IX神经的大鼠的研究结果表明颈动脉体对高压氧时f的增加起主要作用。它们可能受到早期氧中毒诱导的组织中毒性缺氧的刺激。由于完整大鼠和切断IX神经的大鼠在暴露于高压氧时VT的增加幅度都很大且相当相似，所以有人认为VT增加的很大一部分是由高压氧诱导的大脑组织中毒性缺氧引起的乳酸酸中毒刺激中枢化学感受器所致。
