PMID: 11918966Mar 29, 2002Paper

Energy metabolism, stress hormones and neural recovery from cerebral ischemia/hypoxia

Neurochemistry International
A Schurr

Abstract

All the advancements in the understanding of the molecular and cellular processes leading to the great investments in developing neuroprotection against cerebral ischemic/hypoxic damage cannot obscure the simple fact that exhaustion of energy supplies is still at the basis of this disorder. Much has been investigated and postulated over the years about the quick collapse of energy metabolism that follows oxygen and glucose deprivation in the brain. Anaerobic glycolysis, recognized as a pathway of paramount importance in keeping energy supplies, although, at bare minimum, has also presented a dilemma-a significant increase in lactate production during ischemia/hypoxia (IH). The dogma of lactate as a useless end product of anaerobic glycolysis and its postulated role as a detrimental player in the demise of the ischemic cell has persisted for the past quarter of a century. This persistence is due to, at least in part, the well-documented phenomenon termed "the glucose paradox of cerebral ischemia," the unexplained aggravation of postischemic neuronal damage by preischemic hyperglycemia. Recent studies have questioned the deleterious effect of lactic acid, while others even have offered the possibility that this monocarboxylate se...Continue Reading

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