MORPHINE-INDUCED HYPERGLYCEMIA IN THE CAT

¹ Department of Pharmacology, University of Utah College of Medicine, Salt Lake City, Utah

Intraventricular morphine evoked hyperglycemia of similar magnitude and time course, but with only 1/25 to 1/50 of the dose requirement, as that elicited by intravenous administration of the drug. Morphine failed to elicit hyperglycemia after intracisternal injection.

Morphine was at least as effective in eliciting hyperglycemia when injected intraventricularly in a small volume of solution, that localizes in the vicinity of the intraventricular foramen of Monro, as in larger volumes that distribute throughout the entire ventricular system.

Intraventricular nalorphine, in a dose too small to be effective systemically, blocked the hyperglycemic effect of intravenous morphine.

Intraventricular epinephrine was practically ineffective in evoking hyperglycemia. In contrast, lumbar intrathecal injection of epinephrine was even more effective than intravenous administration. Intrathecal epinephrine continued to evoke hyperglycemia after spinal cord ligation above the level of injection.

Ablation of area postrema did not alter hyperglycemic responses elicitable either with morphine or epinephrine.

It is concluded that morphine induces hyperglycemia reflexly through an action on a paraventricular receptor site, probably located near the foramen of Monro. On the other hand, no support could be mustered for a central component in the hyperglycemic action of epinephrine.