thromboxane-b2 and Hypoglycemia

Topics: Alprostadil; beta-Thromboglobulin; Blood Glucose; Blood Platelets; Cholesterol; Diabetes Mellitus, Type 1; Diet; Fatty Acids; gamma-Linolenic Acid; Glycated Hemoglobin; Humans; Hypoglycemia; Insulin; Linolenic Acids; Lipids; Phospholipids; Platelet Aggregation; Prostaglandins E; Thromboxane B2; Triglycerides

Several haemostatic and metabolic variables were monitored during insulin stress tests (ISTs), which were preceded by placebo, nadolol or propranolol ingestion for 10 days. Nadolol administration blocked the rise in plasma factor VIII: RAg concentrations, but no significant changes were observed in platelet aggregation/thromboxane A2 release. Propranolol administration reduced the significance, but not the magnitude, of the plasma factor VIII:Rag rise and also marginally inhibited platelet aggregation/TXA2 release. Both nadolol and propranolol inhibited the hypokalaemia of hypoglycaemia and retarded the recovery of plasma glucose concentrations, probably by inhibiting lipolysis (as indicated by serum nonesterified fatty acid concentrations). Both nadolol and propranolol often masked and delayed the onset of the symptoms of hypoglycaemia. Beta-blockers may exert beneficial effects by modifying haemostatic variables and by preventing hypokalaemia during stressful situations, such as hypoglycaemia or myocardial infarction, both in diabetics and in non-diabetics. However, any benefit must be balanced against the risk of masking, and possibly increasing the incidence of, hypoglycaemia in diabetics.

Topics: Adenosine Diphosphate; Adrenergic beta-Antagonists; Adult; Blood Glucose; Blood Platelets; Blood Pressure; Factor VIII; Fatty Acids, Nonesterified; Female; Humans; Hydrocortisone; Hypoglycemia; Insulin; Kinetics; Male; Nadolol; Platelet Aggregation; Potassium; Propanolamines; Propranolol; Pulse; Thromboxane B2

Topics: Adolescent; Adult; Blood Glucose; Blood Platelets; Diabetes Mellitus, Type 1; Epoprostenol; Fatty Acids, Unsaturated; Humans; Hypoglycemia; Insulin; Thromboxane B2

Prostaglandin synthesis in the brain has been suggested as a component in the control mechanism of the cerebral circulation. During insulin-induced hypoglycemia there is a significant increase in local cerebral blood flow in various brain regions, however, regional loss of autoregulation occurs under these conditions. In the present study the regional distribution of PGE2, TXB2 (the stable metabolite of thromboxane) and 6-keto-PGF1 alpha (the stable metabolite of prostacyclin) was determined in rat brain following decapitation. Three groups of rats were treated with either saline, insulin or 2-deoxyglucose and their brains were rapidly removed one hour later. Samples from the cortex hypothalamus, hippocampus, striatum, nucleus accumbens and cerebellum were assayed by RIA for the content of PGE2, TXB2 and 6-keto-PGF1 alpha. The levels of all three compounds in control rats were the lowest in the striatum and cerebellum, while in the cortex and hippocampus their levels were 4-6 times higher. Insulin had selective effect on the post decapitation levels of prostanoids. It increased PGE2 in the n. accumbens and TXB2 in the hippocampus, and reduced 6-keto-PGF1 alpha and TXB2 in the cortex. 2-DG reduced all PGs in the cortex and 6-keto-PGF1 alpha in the hypothalamus and hippocampus. The results demonstrate that discrete brain areas have a differential capacity to accumulate PGs following decapitation. This capacity is selectively affected by insulin and 2-DG.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Brain Chemistry; Deoxy Sugars; Deoxyglucose; Dinoprostone; Hypoglycemia; Insulin; Male; Prostaglandins; Prostaglandins E; Rats; Thromboxane B2