Sustained elevation of cerebral blood flow after hypoglycaemia in normal man.
During hypoglycaemia, counter-regulatory hormones are released, cognitive function is impaired and cerebral blood flow is increased. In the immediate period after normalisation of blood glucose only counter-regulatory hormones seem to be normalised. The aim of this study was to follow the changes in cerebral blood flow during a prolonged recovery period following moderate hypoglycaemia in normal man. In 15 healthy men, 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 flow was measured by a single photon emission computed tomography camera (SPECT) recording the clearance of intravenously administered xenon-133. Measurements were performed before, at the beginning and at the end 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 this level at all measurements after normalisation of blood glucose. There was no relation between the rate of fall in blood glucose or level of hypoglycaemia and increment in cerebral blood flow or the actual blood flow during hypoglycaemia. The values of plasma adrenaline, serum ACTH, serum cortisol and symptom scores increased significantly during hypoglycaemia. The adrenaline level was back to the basal level at the first measurement after normalisation of blood glucose, while the ACTH level was normalised at the subsequent measurement and the cortisol 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 metabolism influence this vasculatory response.
Department of Internal Medicine, University Hospital, Lund, Sweden.
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Eckert
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Ryding
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Agardh
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D002560:Cerebrovascular Circulation / Q000502:physiology*; D004837:Epinephrine / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007003:Hypoglycemia / Q000503:physiopathology*; D008297:Male; D013990:Tidal Volume; D015899:Tomography, Emission-Computed, Single-Photon; D014655:Vascular Resistance
D001786:Blood Glucose; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone; D004837:Epinephrine