Effect of the anti-motion-sickness medication cinnarizine on central nervous system oxygen toxicity.

Severe seasickness could pose a serious problem in diving, and anti-seasickness medication should therefore be prescribed for the seasickness-susceptible diver. Cinnarizine may be used as a medication if it does not increase the risk of central nervous system (CNS) oxygen toxicity when diving with closed-circuit oxygen or O2-enriched gas mixtures. Twenty-six male, white Sprague-Dawley rats were exposed to high O2 pressures (507 and 608 kPa) before and after cinnarizine ingestion (3.3 mg.kg-1), until the appearance of the first electrical discharge (FED) in the electroencephalogram (EEG) which precedes the clinical convulsions. Each rat was tested on five exposure protocols (control and cinnarizine at 507 kPa O2, control, cinnarizine, and 15 h starvation as a control for cinnarizine at 608 kPa O2) at intervals of at least 2 days or until the EEG connector became detached (a mean of 3.1 exposures per rat). Latency to the FED increased after cinnarizine ingestion in 16 of the 17 pairs of measurements at 507 kPa O2 (by more than 61%, P < 0.002) and in 17 of the 19 pairs of measurements at 608 kPa O2 (by 36%, P < 0.002). There was no significant effect of 15 h starvation. Cinnarizine can be further considered for use in seasickness-susceptible divers as it does not increase the risk of CNS O2 toxicity.