The present study is a further attempt to contribute to an understanding of the essential physiologic mechanisms set up by electric shock and insulin hypoglycemia. Our earlier investigation1 showed that electrically induced convulsions excite in the unanesthetized rat the sympatheticoadrenal and vagoinsulin systems. However, the action on the vagoinsulin system is masked in the normal animal by the predominance of the excitation of the sympatheticoadrenal system, which causes hyperglycemia.
Studies by one of us (E. G.), in collaboration with Ingraham, Moldavsky, Kiely, Kraines and Hamilton,2 have suggested that hypoglycemia likewise produces increased excitability of the sympathetic medullary centers, since the reaction of the blood pressure to anoxia, as well as to carbon dioxide, is greatly increased during hypoglycemia. Moreover, the increased secretion of epinephrine during hypoglycemia is well known.3 That the effect is not restricted to the sympathetic division of the autonomic nervous system is evident from