744 HENRY G. BARBOUR 



glycosurias from the liver, and in the absence of liver glycogen none is 

 excreted. Starkenstein has demonstrated the central mechanism of car- 

 bon monoxid glycosuria and claims by histological and chemical tests to 

 have found the adrenal glands exhausted after carbon monoxid poisoning. 

 In view of the 'work of Kellaway on asphyxia! glycosuria, it seems prob- 

 able that the central action is exerted through the nerves of the liver 

 as well as of the adrenals. 



Other Blood Poisons. Metliemogldbinemia. A number of poisons 

 besides carbon monoxid reduce the oxygen-transporting capacity of the 

 blood. Among the poisons which do this by causing methemoglobinemia 

 are the nitrates, chlorids, bile acids, pyrogallic acid, arsin, piperidin, 

 toluylenediamin, hydroxylamin and others. Antipyretics, phosphorus and 

 some heavy metals produce similar effects, but these constitute a minor 

 part of their action. 



When in its alkaline form, methemoglobin is much more readily con- 

 verted back into oxygen. In accord with this, herbivorous animals appear 

 less susceptible to its formation than the carnivorous. Alkali injec- 

 tions have therefore been suggested in the treatment of methemoglobi- 

 nemia. 



Acid-Base Equilibrium'. Diminished alkalinity of the blood was 

 shown by Hans Meyer, Kraus, Kose and others to be commonly asso- 

 ciated with the blood poisons. 



Protein Metabolism. Nitrogen excretion is increased by relatively 

 small doses of chlorates (Mering(a)). Pyrogallol increases the excretion 

 of nitrogen (Noel Paton), of uric acid (Kiinau) and of neutral sulphur 

 (Bonanni(a)). Pyrodin (Frankel(6)), toluylenediamin, and bile acids 

 (Noel Paton), and large quantities of anilin, quinolin, salicylic acid, etc., 

 also stimulate protein catabolism. Lawrence has shown that nitrites may 

 increase the nitrogen and solids of the urine in man. 



Benzol is a blood poison causing especially destructive changes in the 

 hematopoietic organs, and diminution of the leukocytes and blood plate- 

 lets. Increased excretion of neutral sulphur and of ammonia (Sohn) and 

 a rise in body temperature also occur. 



Carbohydrate Metabolism. Hoffman observed glycosuria from amyl 

 nitrite inhalation. This was associated by Konikof? with the disappear- 

 ance of glycogen from the liver. Araki found the phenomenon associated 

 with lactic acid secretion in both fed and fasted animals. 



Hydrogen sulphid is one of the blood poisons that cause glycosuria 

 (Calm), but since sulphhenioglobin is found only in traces during life, 

 E. Meyer believes the sulphid is directly toxic to the central nervous sys- 

 tem. Other blood poisons causing glycosuria are the chlorates (Stokvis(a) 

 and others) anilin (Brat), nitrobenzol (Magnus-Levy) and orthoni- 

 trophenol-propionic acid (Hoppe-Seyler). 



Bukowski noted in phenol poisoning a rapid disappearance of liver 



