90 



RESPIRATION 



far more easily and exactly than when nothing but the blood 

 pump and the old methods of gas analysis were available. 



The first pair of experiments showed us that Ludwig's old 

 suspicion was correct, and that at the same pressure of CO2 blood 

 takes up considerably more CO2 in the absence than in the presence 

 of oxygen. The upper curve in Figure 25 is the absorption curve 

 for my own blood in the absence of oxygen, and shows that at the 

 physiologically important part of the curve the blood takes up 

 from 5 to 6 volumes per cent more of CO2 if oxygen is absent. We 

 found that the excess of CO2 taken up runs parallel, not to the 

 partial pressure of oxygen, but to the extent to which the oxy- 

 haemoglobin of the blood is dissociated. Saturation of the haemo- 

 globin with CO had just the same effect on the curve as saturation 

 with oxygen. The effect may be due to saturated haemoglobin 

 being a less alkaline substance than reduced haemoglobin, but is 

 more probably dependent on the molecules of reduced haemo- 

 ^ ' globin having a much greater tendency to aggregate than those 

 of saturated haemoglobin. The reasons for this assumption with 

 regard to aggregation were given at the end of last chapter. 

 The aggregated haemoglobin molecules would presumably have 

 less mass influence in keeping out the CO2 from combination with 

 alkali than the unaggregated molecules. 



Let us now see what physiological deductions can be drawn 

 from the absorption curves in Figure 25. Human blood contains 

 about 18 volumes per cent of oxygen, and if all this oxygen were 

 used up in the tissues about 1 5 volumes of CO2 would be formed. 

 But during the using up of the oxygen the absorption curve for 

 CO2 starting from 40 mm. would pass from the lower to the upper 

 curve of Figure 25, following upwards the thick line shown in 

 Figure 26. 



Hence the COg pressure, instead of rising to 80 mm., as would be 

 the case if the lower curve were followed, would only rise to 62 

 mm. Actually, as will be shown later, not more than about a fifth 

 of the oxygen is used up during rest, so the pressure of COg in the 

 mixed venous blood rises only about 5 or 6 mm. This makes it 

 far more easy to understand why the pressure of CO2 in the arte- 

 rial blood should be so exactly regulated as it is. If it had been the 

 case that the resting CO2 pressure in the systemic capillaries were 

 far above the arterial CO2 pressure, the necessity for such exact 

 regulation of the arterial CO2 pressure would have been hard to 

 understand. 



While the venous blood is being aerated in the lungs, the ab- 



