366 RESPIRATION 



haemoglobin percentage and number of red corpuscles fell about 

 20 per cent, and that there was no fall in the case of animals kept 

 in the tunnel at a place where the atmospheric pressure was not 

 increased. It appears, therefore, that the haemoglobin percentage 

 is regulated generally in relation to the oxygen pressure in the 

 arterial blood, and rises or falls according as this pressure is 

 diminished or increased. 



It is easy to see what the physiological advantage will be,' other 

 things being equal, of a rise in the haemoglobin percentage. As 

 the blood passes through the systemic capillaries, its oxygen pres- 

 sure will fall more slowly than usual. Hence although the arterial 

 oxygen pressure is considerably below normal, the venous oxygen 

 pressure will be much more nearly normal, so that the lowering 

 of the oxygen pressure in the tissues is diminshed. There may be 

 much more of available oxygen in the arterial blood at a high 

 altitude than at sea level, but this in itself avails nothing, since it 

 is the pressure, and not the quantity, of oxygen in the blood that 

 counts. To explain the beneficial effects of increased haemoglobin 

 percentage at high altitudes and in other conditions where chronic 

 arterial anoxaemia exists we must consider the effects of the 

 increased haemoglobin on the oxygen pressure in the tissues. At 

 the same time we must bear in mind the influence of increased 

 haemoglobin percentage in diminishing the COg pressure, and 

 therefore the hydrogen ion concentration, in the tissues ; and this 

 brings us to a second factor in acclimatization. 

 — :^ In recent years, it has gradually been shown more and more 

 clearly that at high altitudes the volume of air breathed is in- 

 creased and remains so after acclimatization. This was already 

 more or less evident from the measurements by Zuntz and his 

 colleagues of the volume of air breathed and respiratory exchange 

 at high altitudes, and, as mentioned in Chapter VI, was rendered 

 quite clear by the experiments of Boycott, Ogier Ward, and 

 myself on the alveolar air at low atmospheric pressures. We drew 

 the conclusion that the blood, apart from the CO2 contained in it, 

 becomes less alkaline at low atmospheric pressures, so that less 

 COo is needed to excite the respiratory center. This diminution in 

 the ''fixed'* alkalinity of the blood was already known through 

 titrations. Barcroft then found on the Peak of Teneriffe that in 

 spite of the lowered pressure of COg in the arterial blood, the 

 dissociation curve of the oxyhaemoglobin of the blood in presence 

 of the alveolar COg pressure remains sensibly normal. This also 

 pointed in the same direction. The phenomena did not, however, 



