Children with left-to-right shunt, with and without congestive heart failure, were found to have impaired glucose tolerance tests (GTT). In cyanotic children normal levels of glucose were found in association with abnormally high levels of insulin following oral GTT. Several possible mechanisms are proposed to explain the different glucose tolerance alterations: (1) Suppression of insulin release appeared to partially explain the low levels of insulin in congestive heart failure. This suppression may be related to the high levels of circulating norepinephrine found in these patients. (2) Excessive clearance of insulin by the lung may also be responsible for the reduced arterial insulin levels in patients with left-to-right shunt, and underclearance of insulin for the abnormally higher arterial insulin levels in patients with right-to-left shunts in whom a significant amount of venous blood has bypassed the lung. (3) Hypoxia of the pancreas and the liver in cyanotic patients and those with congestive heart failure may explain the reduction of insulin levels in the hepatic vein following i.v. glucose tolerance tests. An excess production of a glucagonlike gastrointestinal factor in cyanotic children may partially explain the abnormally high levels of insulin following oral GTT.
Effects of epinephrine (10(-5) M) on mechanical performance, glycolysis, glycogenolysis, lipolysis, and metabolism of adenine nucleotides were studied in isolated hypoxic rabbit hearts. The exposure of hearts to hypoxia decreased their mechanical performance and heart rate, but increased their utilization of glucose by 50% and the release of lactate by 139%. Myocardial stores of glycogen and ATP declined by 53 and 84%, respectively, but their breakdown products such as lactate, pyruvate, AMP, and inosine accumulated in these hearts. Myocardial content of free fatty acids decreased, and the amount of glycerol increased in hypoxic hearts. Epinephrine stimulated mechanical performance and heart rate of hypoxic hearts, but decreased myocardial glycogen and ATP even more by 62 and 33%, respectively. Though glucose utilization remained unchanged, the release of lactate increased by 66% from hypoxic hearts treated with epinephrine. However, epinephrine failed to stimulate myocardial lipolysis in hypoxic hearts. These metabolic changes due to epinephrine would lead to accelerated depletion of energetic reserves in hypoxic heart and its earlier deterioration.
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