730 



6. ARSENICALS 



notomy. He concluded that arsenite acts peripherally by increasing hepatic 

 glycogen olysis. This hyperglycemia may be antagonized by insuhn. Gruhzit 

 (1935) reported that only fairly high doses of arsenite cause a rise of blood 

 glucose in dogs and, indeed, Van Dyke had shown that dogs are less respon- 

 sive than rabbits. Oelkers (1937) reinvestigated these matters more thor- 

 oughly and showed that arsenite at 6 mg/kg prolongs the blood glucose 

 levels following injection of glucose (Fig. 6-7), the blood glucose taking 

 5-6 lir to return to normal and in untreated animals only 1.5-2 hr. A similar 



3g GLUCOSE /KG 



0.02 mg EPI /KG 



/ \ 



Fig. 6-7. Effects of arsenite on the blood glucose levels under 



various conditions. The dose was 6 mg/kg AsjOs. The solid curves 



are controls and the dashed curves give the arsenite effects. (From 



Oelkers, 1937.) 



effect on epinephrine-induced hyperglycemia was observed and the hypo- 

 glycemic fall produced by insulin is antagonized by arsenite. Arsenite at 

 near-toxic doses markedly elevates the blood glucose in normal animals; 

 thus 5 mg/kg intravenously almost doubles the blood glucose after 3-4 hr 

 (Oelkers, 1939). This work indicates a definite impairment by arsenite 

 of the utilization of glucose in the tissues, and it is entirely possible that 

 this can account for much of the glycogen loss. Berry and Smythe (1959) 

 concur with this on the basis of their results in mice given 6.25 mg/kg 

 arsenite intraperitoneally (see accompanying tabulation). It is difficult 

 to understand the interference with glucose utilization since one might 

 expect the opposite, and indeed work on isolated tissues has shown that 

 arsenite often augments the uptake of glucose (page 676). The possibility 

 must be considered that these changes are secondary to tissue damage 



