MORPHINE-INDUCED HYPERGLYCEMIA IN THE CAT’2

The literature on morphine-induced hypergly-cemia, up to 1940, has been thoroughly reviewed an(1 interpreted by Krueger, Eddy and Sumwalt (1941, 1943). Although much work has been done in the interim on the regulation of glucose metabolism, our understanding of the hypergly-cemic action of morphine has remained essen-tially unchanged since that time. It was known that morphine evokes a rise in blood sugar in a variety of species regardless of whether the drug causes 1)ehavioral excitation or depression, and irrespective of whether it stimulates or depresses the respiration. Furthermore, it had been estab-lished that the caudal hypothalamus plays an essential pant in the hyperglycemic process and that tile response is mediated through tile sym-pathetic nervous system with primary participa-tion of the adrenal medulla. Thus, the central and efferent components of the reflex mechanism had already been delineated by 1940, but the receptor site of action and affenent limb have vet to be elucidated. This presupposes, of course, that morphine does not act directly on the central integrating ap)aratus concerned in blood sugar regulation. The purposes of this study were, first, to com-pare hyperglycemic effects of morphine by intra-venous and lateral intnacenebroventnicular injec-tion in order to reveal the possible existence of a discrete receptor site in the ventricular system of the brain and, second, to test the postulate that the hyperglycemia is induced through an action ‘This investigation was supported by research grant B-491 from the National Institute of Neuro-logical l)iseases and Blindness