SUSTAINED ELEVATION OF CEREBRAL BLOOD-FLOW AFTER HYPOGLYCEMIA IN NORMAL MAN

During hypoglycaemia, counter-regulatory hormones are released, cognit ive function is impaired and cerebral blood flow is increased. In the immediate period after normalisation of blood glucose only counter-reg ulatory hormones seem to be normalised. The aim of this study was to f ollow the changes in cerebral blood flow during a prolonged recovery p eriod following moderate hypoglycaemia in normal man. In 15 healthy me n, hypoglycaemia was induced by an intravenous infusion of insulin (2. 5 mU/kg per min) to a blood glucose of 2.2 +/- 0.3 mmol/l (mean +/- S. D.) and was kept at this level for 66 +/- 11 min. The cerebral blood f low was measured by a single photon emission computed tomography camer a (SPECT) recording the clearance of intravenously administered xenon- 133. Measurements were performed before, at the beginning and at the e nd of the hypoglycaemic period, as well as 23 +/- 5, 51 +/- 7 and 97 /- 7 min after normalisation of the blood glucose. The basal cerebral blood flow was 50.2 +/- 5.2 ml/100 g per min, increased to 55.6 +/- 4. 9 ml/100 g per min (P < 0.001) during hypoglycaemia, and remained at t his level at all measurements after normalisation of blood glucose. Th ere was no relation between the rate of fall in blood glucose or level of hypoglycaemia and increment in cerebral blood flow or the actual b lood flow during hypoglycaemia. The values of plasma adrenaline, serum ACTH, serum cortisol and symptom scores increased significantly durin g hypoglycaemia. The adrenaline level was back to the basal level at t he first measurement after normalisation of blood glucose, while the A CTH level was normalised at the subsequent measurement and the cortiso l level at the last measurement. In conclusion, the results show that despite normalisation of counter-regulatory hormones and hypoglycaemic symptoms, the cerebral blood flow remains elevated for at least 97 +/ - 7 min following 66 +/- 11 min of moderate hypoglycaemia, indicating that additional factors which, are not coupled to the cerebral metabol ism influence this vasculatory response. (C) 1998 Elsevier Science Ire land Ltd. All rights reserved.