Japanese Journal of Stroke
Online ISSN : 1883-1923
Print ISSN : 0912-0726
ISSN-L : 0912-0726
The effects of blood glucose levels on cerebral blood flow autoregulation in spontaneously hypertensive rats
Kenichiro FujiiSeizo SadoshimaSetsuro IbayashiFujio YoshidaMasatoshi Fujishima
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1986 Volume 8 Issue 5 Pages 363-369

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Abstract

The effects of blood glucose levels on cerebral blood flow (CBF) autoregulation were studied in spontaneously hypertensive rats (SHR). In female SHR at the age of 5 months, blood glucose levels were varied by intravenous administration of streptozotocin (STZ) one week prior the experiment (STZ-diabetes) or intraperitoneal injections of 8% NaCl (normoglycemia), insulin + 8% NaCl (hypoglycemia) or 50% glucose (hyperglycemia) just before the study. Hydrogen clearance method was used to measure local CBF in parietal cortex, thalamus and cerebellar cortex during stepwise reduction of systemic pressure by bleeding.
Average values for mean arterial pressure (MAP) were 185 mmHg in normoglycemia, 179 in hypoglycemia, 174 in hyperglycemia and 165 in STZ-diabetes, and for blood glucose concentration were 133, 40, 465 and 337 mg/dl, respectively. Baseline CBF to cerebral cortex was greater in hypoglycemia (97 ± 17 ml/100g/min) than in normoglycemia (49 ± 4), hyperglycemia (50 ± 4) or STZ-diabetes (62 ± 9). Within each group, CBF autoregulation did not show any regional differences. In intergroup comparison, autoregulatory response in CBF in hyperglycemia and STZ-diabetes was not different from that in normoglycemia. In hypoglycemia, however, local CBF in each region was more reduced during hypotension than in normoglycemia. For example, cortical CBF was reduced to 70% of baseline CBF when MAP was decreased by only 13 ± 1% of baseline MAP in hypoglycemia, but by 37 ± 5% in normoglycemia, of its difference being significant (p<0.01).
These results suggest that either hyperglycemia or short-term diabetes does not alter CBF autoregulation, but hypoglycemia leads to impaired autoregulation. The important role of blood glucose in cerebrovascular reactivity was discussed.

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© The Japan Stroke Society
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