Abstract
CNS‐OT limits the use of hyperbaric O2 (HBO2) clinically and in military diving. We studied the effects of preconditioning (PCs) gas mixtures and dive/seizure history on the latency to seizure (LS) in 118 adult rats implanted with a radio‐transmitter to record EEGs. After ≥1 wk recovery, rats underwent: a) hyperoxic PC at 1‐ 2ATA in pure O2; b) hyperbaric normoxic PC at 2ATA using Heliox/Nitrox; and c) air PC at 1ATA (control) or 2ATA. All PC protocols were conducted 3x, followed 24hr after the last treatment by one dive to 5ATA to seizure. Hyperoxic PC did not provide neuroprotection against seizure, decreasing LS by 51% (2ATA O2) and 42% (1ATA O2). Hyperbaric normoxic PC (2ATA Nitrox/Heliox) decreased LS by 78/89%. Western blot analyses of rat hippocampi suggest that hyperbaric pressure per se (normoxia+inert gases) accelerate onset of CNS‐OT by downregulation of Early Growth Response‐1, an early response gene involved in neuroprotection from oxidative stress. Also, in the absence of PC, rats experiencing 1 seizure/wk over 3–5wk developed a kindling response to HBO2 compared to rats that experienced 1 seizure/wk over 2wk, causing a LS decrease of 74% (4 ATA) and 55% (5 ATA) due to kindling (ONR).
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