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 ‘81. 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 CO, output fell to about a fifth— 
ze. the respiratory quotient became double the normal. On 
returning the caterpillars to air again, the CO, 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 CO, 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 toa half as great 
as would be expected from the output of CO, 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 
