THE MECHANISM OF TISSUE RESPIRATION 165 



and could only be brought back again by the substitution of 

 oxygenated saline. Verworn thought that the first brief recovery 

 of excitability was due to the oxygenless saline washing away 

 the products of fatigue from the tissues, and that the tissues 

 still retained a small amount of intramolecular oxygen. Once 

 this was used up, however, no further recovery of excitability 

 was possible until the tissues were supplied with more oxygen 

 from external sources. 



Even this experimental proof, ingenious at it is, does not 

 finally prove the point at issue, for it is possible that some 

 of the toxic products of fatigue are soluble, and that the 

 removal of these products by oxygenless saline leads to some 

 recovery of excitability. Other of these products may be 

 insoluble, and only be removable after oxidation by free 

 oxygen. 



Still another type of argument in support of the doctrine of 

 intramolecular oxygen is derived from a study of the respiratory 

 quotients yielded by an animal before, during, and after depriva- 

 tion of oxygen. For instance, Thunberg observed that cater- 

 pillars kept in air gave a quotient of *8i. On substituting 

 an atmosphere containing 99/5 per cent, of nitrogen and "5 per 

 cent, of oxygen, their oxygen intake fell to about a tenth of 

 its previous value, whilst their C0 2 output fell to about a fifth — 

 i.e. the respiratory quotient became double the normal. On 

 returning the caterpillars to air again, the C0 2 output increased 

 considerably — though it was never more than half its original 

 value — but the oxygen intake increased in a still greater propor- 

 tion, and respiratory quotients of "64, '67 and 70 were obtained 

 in successive half-hour intervals. Relative to their C0 2 output, 

 the caterpillars were therefore absorbing oxygen at a greater 

 rate than usual, apparently in order to replenish the stock of 

 intramolecular oxygen they had drawn upon during the nitrogen 

 period. The writer obtained similar results with mammalian 

 kidneys, though he found that the extra volume of oxygen 

 absorbed on substituting oxygenated saline for the previous 

 oxygenless perfusion liquid was only a third to a half as great 

 as would be expected from the output of C0 2 during the oxygen- 

 less period. 



But this type of result can likewise be explained on the 

 hypothesis of fatigue products. Such products, if insoluble, may 

 collect in the tissues during the oxygenless period, and require 



