1977 Volume 26 Issue 12 Pages 803-807,838-83
It is well known that the increase of plasma cyclic AMP as a response to insulin-induced hypoglycemia is mediated by the release of endogenous adrenalin. This study was designed to find out if there was any difference in this cyclic AMP response to acute hypoglycemia between normal subjects and asthmatic patients. Regular insulin at the dose of 0.1 unit/kg of body weight was intravenously injected to 8 asthmatic patients (4 male and 4 female, age 14 to 55 years)and 5 normal male subjects (age 23 to 26 years). Blood samples were obtained before, 30, 60, 90 and 120 min after the injection of insulin, and were checked for blood glucose, plasma cortisol and cyclic AMP. Urine was collected for the period of 2 hours prior to and after the injection of insulin and assayed for catecholamines. There was no significant difference in the decrease of blood glucose and the change of plasma cortisol between two groups. No significant increase of urinary noradrenalin was observed in both groups, but urinary adrenalin was markedly increased with the mean increment of 6.16±3.42μg/2hrs and 4.41±3.6μg/2hrs in normal subjects and asthmatic patients, respectively, which had no significant difference between the 2 groups. Plasma cyclic AMP increased significantly from 5.8±3.3 p moles/ml to 13.3±3.5 p moles/ml(p<0.01)at 60 min in normal subjects, while it did not change significantly in asthmatic patients whose basal mean level was 6.2±2.7 p moles/ml. These results suggested that the response to insulin-induced hypoglycemia to increase plasma cyclic AMP was blunted and beta-receptors were suppressed in the studied patients with bronchial asthma.
