770 



HENKY G. BAKBOTJR 



particularly being affected. They believe that the size attained is gov- 

 erned by restrictions placed upon the protein metabolism. 



Carbohydrate Metabolism. According to Lepine and Porteret and to 

 !N"ebelthau antipyretics (antipyrin and acetanilid) are capable of pro- 

 moting the storage of glycogen in both liver and muscles. Starkenstein's 

 claim that antipyretics prevent the mobilization of liver glycogen by 

 epinephrin has been disproved by Mansfield and Purjesz who found that 

 antipyretics exert no demonstrable effect upon the somewhat variable curve 

 of epinephrin hyperglycemia. Noorden examined the claim that salicy- 

 lates decrease the sugar output in diabetes and failed to establish it. 



Hrter (cited by Underbill) observed the production of glycosuria 

 after painting salicylate upon the pancreas of a dog. No other case of 

 glycosuria due to any of this group of drugs appears to have been re- 

 ported. Wacker and Poly have, however, described a rise in the blood 

 sugar content in rabbits and tuberculosis patients after phenacetin and 

 Silberstein found hyperglycemia after giving quiniri to dogs. 



Barbour and Herrmann demonstrated that hyperglycemia (without 

 glycosuria) occurs in both normal and "coli fever" dogs after acetyl- 

 salicylic acid, sodium salicylate, antipyrin and quinin. The following 

 averages were obtained: 



DEXTROSE CONCENTRATION IN BLOOD 



Before 

 Antipyretics 



Maximum 

 After Antipyretics 



Average of 13 normal dogs 0.137 



Average of 10 fevered dogs 0.139 



0.1 8G 

 0.218 



Since the blood of the normal dogs became slightly concentrated and 

 that of the fever dogs diluted by the various drugs the absolute increase 

 in the blood sugar content of the latter was somewhat larger than would 

 appear from the concentration. 



Antipyretic drugs cause no significant changes in the respiratory 

 quotient. 



Water Metabolism. Barbour and Herrmann found after antipyretics 

 a hydremia, as indicated by the hemoglobin content, in a coli fever" but 

 not in normal dogs, as has just been stated. This is induced, at least in 

 part, by the osmotic action of the extra blood sugar. The reason that 

 the hydremia is not seen in the normal dogs appears to be that fever 

 dogs are possessed of a store of available water in the tissues which is 

 not normally present. This contention is supported by Barboiir and 

 Howard's demonstration of an increase in the percentage of blood solids 

 during the initial rise of "coli fever/' without diuresis. Furthermore, 

 water would be liberated with the increased protein catabolism of fever. 



