[Studies on As2O3-induced hyperglycemia (author's transl)]

The mechanisms of hyperglycemia induced by an oral administration of As2O3 were investigated in treated and non-treated rats. The highest level of blood sugar appeared 4 hours after an oral administration of As2O3 15 mg/kg. As2O3-induced hyperglycemia was inhibited with bilateral splanchnicotomy, adrenalectomy or adrenodemedullation. As2O3-induced hyperglycemia was accelerated with bilateral vagotomy. As2O3-induced hyperglycemia was moderately inhibited by depressing the central nervous system activity with barbital sodium. As2O3-induced hyperglycemia was not affected with ephedrine but was inhibited with nicotine, drugs which accelerate catecholamine release of the adrenals. Pretreatment with hexamethonium, torazoline, propranolol or atropine which obstruct the release of catecholamine in adrenals inhibited Aw2O3-induced hyperglycemia. Hepatic glycogen levels decreased 2 hours after As2O3 15 mg/kg administration and returned to normal levels in about 24 hours. These findings indicate that As2O3-induced hyperglycemia was not the result of direct effects of As2O3 on the adrenal but rather was due to effects on the central nervous system.