The secretion of gastric acid in response to a lack of metabolizable glucose. THE SECRETION OF ADRENAL MEDULLARY HORMONES DURING HYPOGLYCEMIA IN INTACT, DECEREBRATE AND SPINAL SHEEP. Reassessment of central neural pathways necessary for adrenaal catecholamine output in response to hypoglycemia. Adrenaline release during insulin hypoglycaemia in the rabbit. Links to PubMed are also available for Selected References. Get a printable copy (PDF file) of the complete article (694K), or click on a page image below to browse page by page. Full textįull text is available as a scanned copy of the original print version. The cells of this receptor like those of the chemoreceptor controlling gastric acid secretion, are activated by an insufficiency of metabolizable glucose. The similarity between this effect and that of the same procedure in preventing the hypersecretion of gastric acid in response to the same stimulus, together with the known fact that hypoglycaemia or the systemic administration of some glucose analogues produce both gastric and adrenal medullary hypersecretion, provides strong presumptive evidence that there exists in the lateral hypothalamic area a chemoreceptor which controls the release of adrenaline. The rise of plasma glucose consequent upon the release of adrenaline following the systemic administration of 3- O-methylglucose is prevented by previous infiltration with lignocaine of the lateral hypothalamic area on both sides.Ģ.
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