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INVITED REVIEW

Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

¹Department of Physiology and Biophysics, Environmental and Hyperbaric Cell Biology Facility, and ²Department of Community Health, Wright State University School of Medicine, College of Science and Mathematics, Dayton, Ohio 45435

As ambient pressure increases, hydrostatic compression of the central nervous system, combined with increasing levels of inspired PO₂, PCO₂, and N₂ partial pressure, has deleterious effects on neuronal function, resulting in O₂ toxicity, CO₂ toxicity, N₂ narcosis, and high-pressure nervous syndrome. The cellular mechanisms responsible for each disorder have been difficult to study by using classic in vitro electrophysiological methods, due to the physical barrier imposed by the sealed pressure chamber and mechanical disturbances during tissue compression. Improved chamber designs and methods have made such experiments feasible in mammalian neurons, especially at ambient pressures <5 atmospheres absolute (ATA). Here we summarize these methods, the physiologically relevant test pressures, potential research applications, and results of previous research, focusing on the significance of electrophysiological studies at <5 ATA. Intracellular recordings and tissue PO₂ measurements in slices of rat brain demonstrate how to differentiate the neuronal effects of increased gas pressures from pressure per se. Examples also highlight the use of hyperoxia (3 ATA O₂) as a model for studying the cellular mechanisms of oxidative stress in the mammalian central nervous system.

anesthesia; carbon dioxide toxicity; free radicals; high-pressure nervous syndrome; membrane potential; nitrogen narcosis; oxidative stress; oxygen toxicity; polarographic oxygen electrode

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