STUDIES ON THE MECHANISM OF MORPHINE HYPERGLYCEMIA THE RÔLE OF THE SYMPATHETIC NERVOUS SYSTEM WITH SPECIAL REFERENCE TO THE SYMPATHETIC SUPPLY TO THE LIVER

¹ From the Departments of Pharmacology and Experimental Surgery, New York University College of Medicine

1. The slight hyperglycemia obtained with morphine in adrenal-inactivated dogs and cats is not abolished after liver denervation.

2. It is not abolished after abdominal sympathectomy.

3. After removal of both lateral sympathetic chains (complete sympathectomy) morphine causes either slight hypoglycemia or no change.

4. Sympathin produced by morphine is the agent responsible for the slight hyperglycemia observed in the (a) adrenal-inactivated, (b) adrenal-inactivated and liver-denervated and (c) abdominal sympathectomized animals respectively.

5. Morphine in the doses given does not act on the liver cells directly to cause a breakdown of liver glycogen.

6. Morphine in the doses given does not suppress the secretion of insulin.

7. It does not bring about secretion of adrenine by acting on the denervated adrenal glands directly.

8. It does not act on the sympathetic nerve endings and collateral sympathetic ganglia.

9. Morphine in producing sympathin must act either on the lateral sympathetic chain or spinal cord or supraspinal centers.²

This article has been cited by other articles:

				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]