Role of catecholamine release in morphine hyperglycemia

¹ Departments of Physiology and Pharmacology, Medical College of Georgia, Augusta, Georgia

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.

This article has been cited by other articles:

				T. M. Doberczak, J. C. Thornton, J. Bernstein, and S. R. Kandall Impact of Maternal Drug Dependency on Birth Weight and Head Circumference of Offspring Arch Pediatr Adolesc Med, November 1, 1987; 141(11): 1163 - 1167. [Abstract] [PDF]

				L. Gould, C.V. Ramana Reddy, Keun-Chang Oh, and Soo Gyum Kim Electrophysiologic Properties of Morphine in Man Angiology, August 1, 1978; 29(8): 579 - 588. [PDF]

				L. Gould, S. Ettinger, A. Carmichael, P. Lord, and P. Hofstra The Use of Phentolamine in Experimental Hemorrhagic Shocka Angiology, May 1, 1970; 21(5): 330 - 335. [PDF]