Effects of Dichloroacetate on Survival Rate, Brain ATP, Lactate, and Water Content Following Cerebral Ischemia in Spontaneously Hypertensive Rats
Previous reports have demonstrated that brain acidosis associated with the accumulation of lactate may aggravate ischemic-hypoxic brain damage [1,2]. Therefore, measures preventing or attenuating lactate accumulation may be protective against the ischemic brain damage. Dichloroacetate (DCA) is known to activate the pyruvate dehydrogenase (PDH) complex in various tissues in vitro by inhibiting PDH kinase  and to reduce serum levels of lactate and pyruvate by its action on PDH . A recent in vivo investigation revealed that DCA significantly lowered the lactate and glucose concentrations of the brain  and that it has therapeutic potential in brain ischemia. Subsequently, Biros and colleages [6–8] have demonstrated that the increase in brain lactate content following incomplete ischemia was reduced by both pre- and post-treatment with DCA. However, the effect of DCA on the neurological outcome of animals subjected to brain ischemia has not been investigated.
KeywordsLactic Acidosis Untreated Group Brain Water Content Neurochemical Pathology Lactate Content
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