Role of catecholamine release in morphine hyperglycemia

Abstract

The mechanism of morphine hyperglycemia was studied in intact and chronically adrenalectomized dogs. Adrenergic blocking agents were used to provide a further analysis of the hyperglycemic action of morphine. Venous hematocrit and plasma specific gravity were measured on the assumption that catecholamines released by morphine could elicit a contraction of the spleen. Morphine administration caused a rise in both sugar and hematocrit; after adrenalectomy, blood sugar and hematocrit showed a much smaller increase. Morphine hyperglycemia was antagonized by dihydroergotamine and dichloroisoproterenol but not by Dibenamine. Since this is the pattern of epinephrine hyperglycemia it was concluded that morphine hyperglycemia is mediated by the release of catecholamines, mainly from the adrenal medulla. Atropine and Artane failed to counteract morphine hyperglycemia. Thus these experiments, as far as the blood sugar is concerned, do not favor the hypothesis that morphine acts through an anticholinesterase mechanism.