I. — PHYSIOLOGY. 1C7 



III Lhe sLagiiaut type of anoxaemia the principal change which is 

 seen to take place is an increase in the quantity of hfemoglobin per 

 cubic millimetre of blood. 



This increase is secondary to a loss of water in the tissues, the 

 result in some cases, as appears from the work of Dale, Richards, and 

 Laidlaw," of a formation of histamine in the tissues. Whether this 

 mcrease of haemoglobin is to be regarded as merely au accidental occur- 

 rence or as a compensation is difficult to decide at present. Houghton's 

 calculations rather sm'prised us by indicating that increased haemoglobin 

 acted less efficiently as a compensatory mechanism than we had 

 expected. This conclusion may have been due to the inaccuracy of 

 our assumptions. I must therefore lemind you that much experimental 

 evidence is required before the assumptions which are made above are 

 anything but assumptions. But, so far as the evidence available at the 

 present time can teach any lesson, that lesson is this: The only way 

 of dealing satisfactorily with the anoxic type of anoxaemia is to abohsh 

 it by in some way supplying the blood with oxygen at a pressm'e suffi- 

 cient to saturate it to the normal level. 



It has been maintained strenuously by the Oxford school of physio- 

 logists that Nature actually did this ; that when the partial pressure in 

 the air-cells of the lung was low the cellular covering of that organ 

 could clutch at the oxygen and force it into the blood at an unnatural 

 pressure, creating a sort of forced draught. This theory, as a theory, 

 has much to recommend it. I am sorry to say, however, that I cannot 

 agree with it on the present evidence. I will only make a passing 

 allusion to the experiment which I performed in order to test the theory, 

 living for six days in a glass respiration-chamber in which the partial 

 pressure of oxygen was gradually reduced until it was at its lowest — 

 about 45 mm. Such a pressure, if the lung was incapable of creating 

 what I have termed a forced draught, would mean an oxygen pressm-e 

 of 38-40 mm. of mercury in the blood, a change sufficient to make 

 the arterial blood quite dark in colour, whereas, did any considerable 

 forced draught exist, the blood in the arteries would be quite bright in 

 colour. Could we but see the blood in the arteries, its appearance alone 

 would almost give the answer as to whether or no oxygen was forced, 

 or, in technical language, secreted, through the lung wall. And, of 

 course, we could see the blood in the arteries by the simple process of 

 cutting one of them open and shedding a little into a closed glass tube. 

 To the surgeon this is not a difficult matter, and it was, of course, done. 

 The event showed that the blood was dark, and the most careful analyses 

 failed to discover any evidence that the body can force oxygen into 

 the blood in order to compensate for a deficiency of that gas in the air. 



Yet the body is not quite powerless. It can, by breathing more 

 deeply, by increasing the ventilation of the lungs, bring the pressure 

 of oxygen in the air-cells closer to that in the atmosphere breathed 

 than would otherwise be the case. I said just now that the oxygen 

 in my lungs ckopped to a minimal pressure of 45 mm. ; but it did not 

 remain at that level. \Yhen I bestirred myself a little it rose, as the 

 result of increased ventilation of the lung, to 56 mm., and at one time, 

 when I was breathing through valves, it reached 68 mm. Nature will 



