EFFECTS OF CEKTAIN DKUGS AND POISONS 745 



glycogen and Borchardt (cited by Allen) found glycosuria in rabbits after 

 0.5 c.c. subcutaneous injections. 



Piperidin glycosuria was shown by Underbill to be accompanied by 

 hyperglycemia and asphyxial in origin, disappearing under oxygen ad- 

 ministration. Biihl and others produced glycosuria by inhalation of 

 acetone, also an asphyxial poison. 



Chlorid Excretion. Kast found, as in carbon monoxid poisoning, an 

 increased chlorid excretion after pyrogallol and toluylenediamin in 

 chlorid-poor animals. 



Syntheses. Amyl nitrite inhibits ethereal sulphate synthesis (Katsu- 

 yama) and certain aromatic diamins which are also blood poisons were 

 found by Pohl(o.) 4o inhibit the synthesis of hippuric acid, but not of 

 glycuronic or of ethyl-sulphuric acid. 



Cyanids. A type of asphyxial poisoning occurs in which neither 

 the external respiratory mechanism nor the oxygen-transporting capacity 

 of the blood is disturbed. 



Claude Bernard pointed out that the venous blood in cyanid poison- 

 ing is red, although the other changes are those of asphyxia. He deter- 

 mined that the action of cyanid upon the blood is not the same as that of 

 carbon monoxid since blood when mixed with cyanid will not turn red 

 in the absence of air. In other words, the red color of the venous blood 

 was ascribed simply to oxyhemoglobin. This was conclusively proven 

 when Zeynek showed that at body temperature hemoglobin will not unite 

 with cyanid, and oxyhemoglobin unites with it only after heating for 

 several hours. 



That the blood returns from the tissues still laden with oxygen was 

 shown by Geppert(&), who obtained the following oxygen determinations 

 in cyanid-poisoned rabbits : 



VOLUMES PER CENT OXYGEN 



Arterial blood Venous blood Difference 



12.2 10.9 1.3 



13.0 12.4 0.6 



In various ways this investigator showed that the power of the blood 

 to attach or to release oxygen is in no wise interfered with during cyanid 

 poisoning. 



Geppert showed further that the first effect of moderate doses of prus- 

 sic acid upon the oxygen consumption of rabbits, cats, and dogs is one of 

 augmentation, which is soon followed by a marked diminution. The 

 return to normal in non-lethal poisoning is preceded by another wave of 

 somewhat high oxygen intake. These stages are illustrated in the follow- 

 ing table : 



