Extracellular potassium activity and cerebral blood flow during moderate hypoglycemia in anesthetized dogs
Sieber, F.E.; Wilson, D.A.; Hanley, D.F.; Traystman, R.J.
American Journal of Physiology 264(6 Pt 2): H1774-H1780
1993
ISSN/ISBN: 0002-9513 PMID: 8322905 Document Number: 406676
Moderate hypoglycemia (MH) may be associated with blunting of cerebral hypocapnic vasoconstriction. Coincident with this change, electroencephalogram (EEG) flattening occurs. Previous reports show that brain extracellular potassium activity ((K+)-o) increases in association with the onset of isoelectricity during severe hypoglycemia and that K+ increases cause pial vessel vasodilation. Using a model of MH, we tested the hypothesis that increases in (K+)-o ( apprx 15 mM) correlate with blunting of cerebral hypocapnic vasoconstriction. Cerebral blood flow (CBF), (K+)-o, and EEG were measured during normocapnia (arterial PCO-2 (Pa-CO-2) = 35 Torr)) and hypocapnia (Pa-CO-2 = 15 Torr) in MH ( lt 2 mM) and normoglycemic dogs. During MH, increases in (K+)-o occurred in association with EEG flattening (from 4.2 +- 0.5 to 13.8 +- 3.8 mM). During normoglycemia and MH without (K+)-o elevations, hypocapnic vasoconstriction occurred. (K+)-o elevations with MH were associated with increased CBF and decreased vascular resistance (146 +- 5 and 42 +- 2% of control, respectively) during normocapnia, and blunting of cerebral hypocapnic vasoconstriction (93 +- 16% normocapnic control) when (K+)-o increased during hypocapnia. This study shows that increases in (K+)-o during MH are necessary for both normocapnic increases in CBF and blunting of cerebral hypocapnic vasoconstriction. Increases in (K+)-o may represent a mechanism for decreases in cerebral vascular resistance during MH.