Abstract
With a level of hypoglycemia (1-1.5 mM) that does not alter cerebral O2 uptake and glucose uptake in dogs, induction of hypocapnia may cause severe electroencephalographic (EEG) abnormalities. The aim of this study was to determine the effect of hypoglycemia (blood glucose = 1.1 ± 0.1 mM) and hypocapnia (arterial PCO2 = 15 ± 1 mmHg) on cerebral ATP, phosphocreatine, and intracellular pH (pH(i); 31P magnetic resonance spectroscopy), cerebral blood flow (CBF; radiolabeled microspheres), global O2 uptake, and glucose uptake in anesthetized dogs. Neither hypoglycemia nor hypocapnia alone altered brain high-energy phosphates, pH(i), O2 or glucose uptake or caused major EEG abnormalities. Hypocapnia alone decreased CBF to 62 ± 4% of control. The combination of hypoglycemia and hypocapnia did not decrease CBF (85 ± 6% of control), and O2 and glucose uptake were unchanged. During hypocapnic hypoglycemia, isoelectric EEG was seen in 40% of animals, ATP and phosphocreatine decreased to 38 ± 12 and 43 ± 12% of control, respectively, while pH(i) increased from 7.13 ± 0.05 to 7.43 ± 0.09. The increase in pH(i) was related reciprocally to the decrease in venous PCO2, indicating little change in intracellular bicarbonate concentration ([HCO3/-](i)). With normoglycemic hypocapnia, in contrast, estimated [HCO3/-](i) decreased 57 ± 1%. These data suggest that active regulation of pH(i) during normoglycemic hypocapnia is impaired during hypoglycemic hypocapnia associated with decreased ATP.
Original language | English (US) |
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Pages (from-to) | H1864-H1871 |
Journal | American Journal of Physiology - Heart and Circulatory Physiology |
Volume | 263 |
Issue number | 6 32-6 |
DOIs | |
State | Published - 1992 |
Keywords
- cerebral blood flow
- cerebral metabolism
- glucose
- insulin
- phosphorus-31 nuclear magnetic resonance
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine
- Physiology (medical)