Role of k+ in regulating hypoxic cerebral blood flow in the rat:
effect of glibenclamide and ouabain.
Reid, John M., and David J. Paterson.
University Laboratory of Physiology, Parks Road, Oxford, OX1 3PT,
United Kingdom
APStracts 2:0302H, 1995.
John M. Reid and David J. Paterson. Role of K+ in regulating hypoxic
cerebral blood flow in the rat: effect of glibenclamide and ouabain.
We assessed the role of extracellular potassium ([K+]e) on the
increase in cerebral blood flow (CBF) during hypoxia, and tested
whether it was affected by a sulphonylurea or ouabain. Cortical CBF
was measured using the hydrogen clearance technique in enflurane
-anesthetized rats and local [K+]e was measured with K+
microelectrodes adjacent to the hydrogen electrode. Eucapnic hypoxia
(PaO2 35-40 Torr) increased CBF two-fold and caused a modest rise in
[K+]e (from 2.9+/-0.2 to 3.7+/-0.2 mM; mean arterial blood pressure,
ABP, 86+/-5 mmHg). If ABP fell below 70 mmHg during hypoxia, no
increase in CBF was seen whereas [K+]e increased to >20 mM.
Glibenclamide (10-100 [mu]M, intracortically) attenuated [K+]e and
CBF during hypoxia (ABP 75 mmHg, p<0.01). Ouabain (20-1000
[mu]M) increased [K+]e, however it did not remove the hypoxic-induced
rise in [K+]e. We conclude that glibenclamide-sensitive potassium
channels contribute to the accumulation of [K+]e during hypoxia,
although an increase in CBF during hypoxia can occur without a marked
rise in [K+]e. Furthermore, if ABP falls below the lower limit of
autoregulation during hypoxia there is no increase in CBF, yet there
is a large increase in [K+]e.
Received 28 April 1995; accepted in final form 13 July 1995.
APS Manuscript Number H399-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 July 1995.