Ventilation in intact and glossopharyngeal nerve sectioned anaesthetized rats exposed to oxygen at high pressure.

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.