100 THE ROYAL SOCIETY OF CANADA 



Particular attention is given in the present research to the possible 

 cause of the hyperpnœa. With this object in view the behaviour of 

 the percentage of carbon dioxide in the alveolar air and arterial blood 

 as well as the hydrogen-ion concentration and the percentage of lactic 

 acid in the latter have been compared with the respiratory behaviour 

 of the animal. The acid excretion by way of the urine has also been 

 observed. 



It has been found that the above-mentioned values remain toler- 

 ably constant in the animals which do not become hyperpnœic, but 

 that in those which do so the alveolar-C02 steadily declines, accom- 

 panied or followed by a decline in blood carbonates and by a decided 

 increase in the hydrogen-ion concentration and lactic acid content of 

 the arterial blood. These blood changes indicate that unoxidised 

 acid, lactic, has accumulated in the blood and the main question to be 

 considered is whether the hyperpnœa is the result of the accumulation 

 of acid or whether the acid accumulates because of hyperpnœa. Con- 

 cerning the first hypothesis the close attention which has been given 

 in recent years to the condition known as acidosis has shown that there 

 are three characteristic signs of the condition: first, a decrease in the 

 percentage of carbon dioxide in the alveolar air ; secondly, a decrease in 

 the ability of the blood to combine with this gas, and thirdly, an in- 

 creased excretion of free acid by the kidney. Now it will be noted that 

 the first two of these characteristics are very prominently affected in 

 those decerebrate cats which became hyperpnœic, and that the third — 

 acid excretion in the urine — in the cases in which it could be measured, 

 remained decidedly higher in the hyperpnœic animals than in those 

 that breathed normally. If we add to these indirect evidences of an 

 acidosis condition the further evidence afïorded by a determination of 

 the hydrogen-ion concentration of the arterial blood there seems little 

 doubt that an intoxication by acid must have been the cause of the 

 hyperpnœa. As to the nature and source of this acid there is evidence 

 that it was lactic acid — large percentages being found in the arterial 

 blood — ^which may have been derived from the plastic tonus of the 

 muscles of the decerebrate animals, for this condition, though present 

 in all the animals, was especially prominent in those that became 

 hyperpnœic. It has been shown by Roaf (Quart. Journ. Exp. Physiol., 

 912, V, 31-53) that the gaseous metabolism of decerebrate cats is no 

 greater than that of animals whose muscles are paralysed by curare, 

 which indicates that very little energy can be expended notwithstand- 

 ing the permanently contracted state of the muscles. 



If we accept the modern view which is the outcome of the work of 

 F. Gowland Hopkins and Fletcher (Proc. Roy. Soc. Lond., 1917, Ser. 



