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Recent experimental evidences indicate that pyruvate, the final metabolite ofglycolysis, has a remarkable protective effect against different types of braininjury. The purpose of this study was to assess the neuroprotective effect andthe neurological outcome after pyruvate administration in a model of ischemicstroke induced by permanent middle cerebral artery occlusion (pMCAO) in rats.Three doses of pyruvate (250, 500 and 1000 mg/kg, i.p.) or vehicle wereadministered intraperitoneally 30 min after pMCAO. In other set of experiments,pyruvate was given either before, immediately after ischemia or in a long-termadministration paradigm. Functional outcome, mortality and infarct volume weredetermined 24 h after stroke. Even when the lowest doses of pyruvate reducedmortality and neurological deficits, no concomitant reduction in infarct volumewas observed. The highest dose of pyruvate increased cortical infarction by 27%when administered 30 min after pMCAO. In addition, when pyruvate was givenbefore pMCAO, a significant increase in neurological deficits was noticed.Surprisingly, on the contrary of what was found in the case of transient globalischemia, present findings do not support a great neuroprotective role forpyruvate in permanent focal cerebral ischemia, suggesting two distinctmechanisms involved in the effects of this glycolytic metabolite in theischemic brain.

Effects of pyruvate administration on infarct volume and neurological deficits following permanent focal cerebral ischemia in rats