Serum enzyme rise after hypoxia and effect of autonomic blockade

¹ Laboratory of Pathology and Histochemistry and Laboratory of Physical Biology, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Maryland

Dogs exposed for 4 hours to a simulated altitude of 32,000 feet showed hyperglycemia and a sharp rise in serum glutamic oxalacetic transaminase (SGO-T), serum glutamic pyruvic transaminase (SGP-T), serum lactic dehydrogenase (SLD), and serum alkaline phosphatase (SAk-P). Hyperglycemia reached a peak in about 6 hours and subsided within 24 hours. Other elevations reached a peak in 6–24 hours and subsided in 3–7 days. The increases in SGO-T, SGP-T and SLD were diminished by the adrenergic blocking agent phenoxybenzamine (Dibenzyline) and the hyperglycemia by the ganglionic blocking agent chlorisondamine dimethochloride (Ecolid). These findings support the view that high altitude hypoxia causes hyperglycemia by releasing catecholamines from the adrenal medulla and increases certain serum enzyme values by increasing selectively cellular permeability to such enzymes. Pretreatment with epinephrine-in-oil before an exposure greatly increased the serum enzyme rise at 24 hours but diminished the 6-hour rise of SGO-T; this suggests partial inactivation of some serum enzymes by an excess of metabolites associated with hypoxia and/or epinephrine.

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