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• W2025405502 startingPage "133" @default.
• W2025405502 abstract "Purpose of review Energy metabolism is increasingly recognized as a key factor in the pathogenesis of acute brain injury (ABI). We review the role of cerebral lactate metabolism and summarize evidence showing that lactate may act as supplemental fuel after ABI. Recent findings The role of cerebral lactate has shifted from a waste product to a potentially preferential fuel and signaling molecule. According to the astrocyte–neuron lactate shuttle model, glycolytic lactate might act as glucose-sparing substrate. Lactate also is emerging as a key signal to regulate cerebral blood flow (CBF) and a neuroprotective agent after experimental ABI. Clinical investigation using cerebral microdialysis shows the existence of two main lactate patterns, ischemic – from anaerobic metabolism – and nonischemic, from activated glycolysis, whereby lactate can be used as supplemental energy fuel. Preliminary clinical data suggests hypertonic lactate solutions improve cerebral energy metabolism and are an effective treatment for elevated intracranial pressure (ICP) after ABI. Summary Lactate can be a supplemental fuel for the injured brain and is important to regulate glucose metabolism and CBF. Exogenous lactate supplementation may be neuroprotective after experimental ABI. Recent clinical data from ABI patients suggest hypertonic lactate solutions may be a valid therapeutic option for secondary energy dysfunction and elevated ICP." @default.
• W2025405502 created "2016-06-24" @default.
• W2025405502 creator A5000775806 @default.
• W2025405502 creator A5089424249 @default.
• W2025405502 date "2014-04-01" @default.
• W2025405502 modified "2023-10-09" @default.
• W2025405502 title "Lactate and the injured brain" @default.
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• W2025405502 doi "https://doi.org/10.1097/mcc.0000000000000072" @default.
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