RT Journal Article
SR Electronic
T1 PARTICIPATION OF A CNS-THYROID NEURAL PATHWAY IN EPINEPHRINE-INDUCED HYPERGLYCEMIA IN THE CAT
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 325
OP 331
VO 152
IS 2
A1 Louis P. Gangarosa
A1 Victor Distefano
YR 1966
UL http://jpet.aspetjournals.org/content/152/2/325.abstract
AB Two successive doses of epinephrine injected into normal or sham-operated cats evoked similar increases in blood glucose. Hyperglycemic responses to epinephrine (EHG) were attenuated in high spinal cats, thus verifying results reported previously. This observation is best explained by assuming an interruption of an epinephrine-activated hyperglycemic neural pathway to the periphery. Since high thoracic spinal section, bilateral thoracocervical sympathectomy, thyroid denervation and thyroidectomy attenuated the EHG, it is postulated that the hyperglycemic pathway emerges from the spinal cord high in the thoracic region, ascends in the sympathetic chain and innervates the thyroid gland. Attenuated epinephrine-induced hyperglycemia was not noted after low thoracic spinal cord section (below T4), pancreatectomy, hepatic denervation or hypophysectomy. Occlusion of the thyroid vein attenuated by EHG, suggesting the release of a thyroid hyperglycemic factor. The Williams & Wilkins Comapny