STUDIES IN THE REGULATION OF BLOOD-SUGAR CONCENTRATION IN CRUSTACEANS. II. EXPERIMENTAL HYPERGLYCEMIA AND THE REGULATORY MECHANISMS

¹ Reed College, Portland, Oregon, and the Marine Biological Laboratory, Woods Hole, Mass.

1. Asphyxia of normal Astacus and Callinectes results in marked increase in concentration of blood-sugar; such increase is mediated by sinus glands located in the eyestalks, for after removal of these glands hyperglycemia does not occur after asphyxia. Hyperglycemic response to asphyxia is part of a reflex mechanism; it does not occur following denervation of the sinus glands.

2. Chloroform anesthesia in Astacus similarly evokes rises in glycemic level which fail to occur after sinus gland removal. Since anesthesia brings about cardiac arrest, the resultant anoxia may be the basic explanation of the anesthesiainduced hyperglycemia.

3. Adrenaline, in doses from 1 to l00, causes hyperglycemia in normal Astacus, but injection into sinus-glandless crayfish shows either no rise in the concentration of blood-sugar, or a very slight one. Similar injections into Callinectes result in marked hyperglycemia in normal individuals, in animals with denervated sinus glands, in sinus-glandless and also in eyestalkless individuals.

4. The results of this study indicate the presence of an excitement hyperglycemia in these crustaceans, ensuing from release of diabetogenic hormone from the sinus glands. The effects of adrenaline in Callinectes may be due to its action on glandular tissue outside of the eyestalk, bringing about secretion of diabetogenic hormone (in addition to its effect on the sinus glands), or to its action on carbohydratestoring tissue resulting in release of glucose.