AJP - Endocrinology and Metabolism, Vol 245, Issue 4 384-E390, Copyright © 1983 by American Physiological Society
Effect of blood pH and ischemia on kinetic constants for cerebral glucose transport
J. M. Yanushka, D. J. Costello and D. D. Gilboe
In 117 experiments, the isolated canine brain was subjected either to 4-min
pulses with blood ranging from pH 6.8 to 7.8, 30 min of hypoxia (PaO2 30
mmHg or 40 mmHg), or 30 min of complete ischemia followed by 60 min of
perfusion with normal oxygenated blood. Unidirectional and net glucose
fluxes were measured under all experimental conditions, and kinetic
constants were calculated for unidirectional transport at each pH and after
ischemia. In brains perfused with blood having a PaO2 of 30 or 40 mmHg, we
observed a 58 and a 55% increase, respectively, in the net flux; however,
there was no significant change in the unidirectional flux either during
hypoxia or during the recovery period. Exposure of the brains to blood with
a pH of 6.8, 7.0, and 7.2 had no effect on the unidirectional flux;
however, as pH was raised above 7.4 both the Km and Vmax increased,
reaching a maximum of 12.06 +/- 2.34 mM and 2.38 +/- 0.28 mumol X g-1 X
min-1, respectively, at pH 7.8. The V/K ratio was unchanged. After 30 min
of ischemia, there was a significant change (P less than 0.05) in the Km of
the unidirectional glucose transport process from a control value of 5.84
+/- 1.75 mM to 17.40 +/- 5.50. These studies suggest that unidirectional
flux is impaired after ischemia due to a decrease in the carrier's affinity
for glucose; however, the observed changes are apparently unrelated to a
fall in tissue pH. A similar mechanism is believed to be responsible for
the decrease in unidirectional glucose flux after hypoxia.
