524 XI. HEMOGLOBIN CATABOLISM, I 



rarely than hemiglobin. Blood rarely contains more than 10% of 

 sulfhemoglobin. It is usually present only in the corpuscles, but in 

 severe bacteremia it may be found in the plasma; so far it has never 

 been reported in the urine. Large amounts can frequently be found 

 in cases of phenacetin misuse, and have been observed by us in one 

 case of quack therapy with sulfur. 



The actual agent of sulfhemoglobin production is always hydrogen 

 sulfide, produced in the intestine by the action of bacteria on food 

 residues and absorbed from the large intestine. Normally this is 

 excreted in the lungs or destroyed, but if present in excess, or in the 

 presence of catalysts which accelerate its action on hemoglobin, 

 sulfhemoglobin is produced. Of all sulfur compounds only elementary 

 sulfur, sulfides, or thiosulfates produce sulfhemoglobin directly 

 (224-5). Cysteine is inactive, and in the action of magnesium sulfate 

 or sulfonamides their sulfur content is of no significance. Magnesium 

 sulfate may cause hydrogen sulfide production in the intestine, and 

 the sulfonamides act as catalysts of sulfhemoglobin formation like 

 other aromatic amino compounds. The catalytic action of phenyl- 

 hydrazine and other amino compounds on sulfhemoglobin formation 

 in vitro was first observed by van den Bergh and Wieringa (24-0). 

 Smith {2577) found 0.1-1.5 g. of sulfhemoglobin per 100 ml. of blood 

 after sulfanilamide, while sulfapyridine produced little or none. 



The distinction between sulfhemoglobin and hemiglobin is of 

 clinical importance (c/. Chapter X, Section 7.2.), since the conversion 

 of hemoglobin into sulfhemoglobin is irreversible and the pigment 

 loses its oxygen-carrying function, while hemrglobin is reduced in 

 the blood (c/. 398,1427,2121,2617,3003) and becomes again function- 

 ally active. The sulfhemoglobin-containing cells are not destroyed in 

 the circulation more rapidly than normal erythrocytes {1427) and 

 persist for several months. 



The intracorpuscular sulfhemoglobin cannot therefore be a pre- 

 cursor of intracorpuscular bile pigment formation and erythrocyte 

 breakdown. 



5.3. Intracellular Changes after Phenylhydrazine 



The earlier literature on the action of phenylhydrazine has been 

 reviewed by Von Oettingen {2067). The formation of a characteristic, 

 hitherto unknown, brown pigment with well-defined absorption by 

 the action of phenylhydrazine on oxyhemoglobin was first noticed 

 by Hoppe-Seyler {1340) in 1885. The brown pigment in the cells 



