Abstract 486 Endocrinology I Poster Symposium, Saturday, 5/1

Previous work has demonstrated a relationship between increased levels of epinephrine during experimental hypoglycemia and cognitive dysfunction. To assess the effect of hypoglycemia independent of epinephrine, we used adrenergic blockade to prevent the α and β adrenergic actions of epinephrine and norepinephrine stimulated by hypoglycemia. Specifically, propranolol (β adrenergic blocker) was infused at a dose of 1.4 µg/kg/min × 2 min, and phentolamine (α adrenergic blocker) was infused at a dose of 7.1 µg/kg/min after a loading dose of 71 µg/kg/min × 2 min in normal saline. Twenty-three diabetic subjects (mean age = 17.6 yrs) participated in two hypoglycemic clamps: one standard clamp in which mild hypoglycemia (3.3 mmol/L) was maintained for 45 minutes prior to cognitive assessment, and one with a α and β adrenergic blockade. Sustained attention was measured with the Digit Vigilance Test, mental flexibility was assessed with Trail Making B, and decision-making efficiency was assessed with the computerized Letter Rotation Test. Adrenergic blockade resulted in a significant decrease in pulse and blood pressure (p < .001), but there was no statistically significant effect on the increment of anxiety symptoms. In addition, it did not prevent the occurrence of hypoglycemia-associated cognitive deterioration on any measure. We conclude that the adrenergic hormonal changes occurring during hypoglycemia are markers of CNS autonomic changes, but do not have any major direct effects on factors influencing the deterioration of cognitive function during mild hypoglycemia in diabetes. (Figure)

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