Stroke, Vol 21, 1458-1463, Copyright © 1990 by American Heart Association
S Gueldry, C Marie, L Rochette and J Bralet
We assessed the effect of 1,3-butanediol on cerebral energy metabolism and
edema after inducing multifocal brain infarcts in 108 rats by the
intracarotid injection of 50-microns carbonized microspheres. An ethanol
dimer that induces systemic ketosis, 25 mmol/kg i.p. butanediol was
injected every 3 hours to produce a sustained increase in the plasma level
of beta-hydroxybutyrate. Treatment significantly attenuated
ischemia-induced metabolic changes by increasing the concentrations of
phosphocreatine, adenosine triphosphate, and glycogen and by reducing the
concentrations of pyruvate and lactate. Lactate concentration 2, 6, and 12
hours after embolization decreased by 13%, 44%, and 46%, respectively.
Brain water content increased from 78.63% in six unembolized rats to 80.93%
in 12 saline-treated and 79.57% in seven butanediol-treated rats 12 hours
after embolization. (p less than 0.05). The decrease in water content was
associated with significant decreases in the concentrations of sodium and
chloride. The antiedema effect of butanediol could not be explained by an
osmotic mechanism since equimolar doses of urea or ethanol were
ineffective. Our results support the hypothesis that the beneficial effect
of butanediol is mediated through cerebral utilization of ketone bodies
arising from butanediol metabolism, reducing the rate of glycolysis and the
deleterious accumulation of lactic acid during ischemia.
ARTICLES
Beneficial effect of 1,3-butanediol on cerebral energy metabolism and edema following brain embolization in rats
Laboratoire de Pharmacodynamie et Physiologie Pharmaceutique, Faculte de Pharmacie, Dijon, France.