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REVIEW
Year : 2021  |  Volume : 11  |  Issue : 4  |  Page : 158-173

Effects of lactate and carbon monoxide interactions on neuroprotection and neuropreservation


Department of Surgery and Pediatrics, Drexel University College of Medicine, Philadelphia, PA, USA

Correspondence Address:
Vicki L Mahan
Department of Surgery and Pediatrics, Drexel University College of Medicine, Philadelphia, PA
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2045-9912.318862

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Lactate, historically considered a waste product of anerobic metabolism, is a metabolite in whole-body metabolism needed for normal central nervous system (CNS) functions and a potent signaling molecule and hormone in the CNS. Neuronal activity signals normally induce its formation primarily in astrocytes and production is dependent on anerobic and aerobic metabolisms. Functions are dependent on normal dynamic, expansive, and evolving CNS functions. Levels can change under normal physiologic conditions and with CNS pathology. A readily combusted fuel that is sshuttled throughout the body, lactate is used as an energy source and is needed for CNS hemostasis, plasticity, memory, and excitability. Diffusion beyond the neuron active zone impacts activity of neurons and astrocytes in other areas of the brain. Barriergenesis, function of the blood-brain barrier, and buffering between oxidative metabolism and glycolysis and brain metabolism are affected by lactate. Important to neuroprotection, presence or absence is associated with L-lactate and heme oxygenase/carbon monoxide (a gasotransmitter) neuroprotective systems. Effects of carbon monoxide on L-lactate affect neuroprotection – interactions of the gasotransmitter with L-lactate are important to CNS stability, which will be reviewed in this article.


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