Effects of nitrogen and helium on CNS oxygen toxicity in the rat.

The contribution of inert gases to the risk of central nervous system (CNS) oxygen toxicity is a matter of controversy. Therefore, diving regulations apply strict rules regarding permissible oxygen pressures (Po(2)). We studied the effects of nitrogen and helium (0, 15, 25, 40, 50, and 60%) and different levels of Po(2) (507, 557, 608, and 658 kPa) on the latency to the first electrical discharge (FED) in the EEG in rats, with repeated measurements in each animal. Latency as a function of the nitrogen pressure was not homogeneous for each rat. The prolongation of latency observed in some rats at certain nitrogen pressures, mostly in the range 100 to 500 kPa, was superimposed on the general trend for a reduction in latency as nitrogen pressure increased. This pattern was an individual trait. In contrast with nitrogen, no prolongation of latency to CNS oxygen toxicity was observed with helium, where an increase in helium pressure caused a reduction in latency. This bimodal response and the variation in the response between rats, together with a possible effect of ambient temperature on metabolic rate, may explain the conflicting findings reported in the literature. The difference between the two inert gases may be related to the difference in the narcotic effect of nitrogen. Proof through further research of a correlation between individual sensitivity to nitrogen narcosis and protection by N(2) against CNS oxygen toxicity in rat may lead to a personal O(2) limit in mixed-gas diving based on the diver sensitivity to N(2) narcosis.

Optimal oxygen pressure and time for reduced bubble formation in the N2-saturated decompressed prawn.

Bubbles that grow during decompression are believed to originate from preexisting gas micronuclei. We showed that pretreatment of prawns with 203 kPa oxygen before nitrogen loading reduced the number of bubbles that evolved on decompression, presumably owing to the alteration or elimination of gas micronuclei (Arieli Y, Arieli R, and Marx A. J Appl Physiol 92: 2596-2599, 2002). The present study examines the optimal pretreatment for this assumed crushing of gas micronuclei. Transparent prawns were subjected to various exposure times (0, 5, 10, 15, and 20 min) at an oxygen pressure of 203 kPa and to 5 min at different oxygen pressures (PO2 values of 101, 151, 203, 405, 608, and 810 kPa), before nitrogen loading at 203 kPa followed by explosive decompression. After the decompression, bubble density and total gas volume were measured with a light microscope equipped with a video camera. Five minutes at a PO2 of 405 kPa yielded maximal reduction of bubble density and total gas volume by 52 and 71%, respectively. It has been reported that 2-3 h of hyperbaric oxygen at bottom pressure was required to protect saturation divers decompressed on oxygen against decompression sickness. If there is a shorter pretreatment that is applicable to humans, this will be of great advantage in diving and escape from submarines.

Use of a mass spectrometer for direct respiratory gas sampling from the hyperbaric chamber.

BACKGROUND: When conducting respiratory gas measurements during hyperbaric chamber research, it is preferable to carry out gas concentration analysis by mass spectrometry. Gas samples for the mass spectrometer are normally taken from a bypass flow exiting the high pressure chamber to the ambient atmosphere. Under these conditions, mixing in the sampling line smoothes the concentration profile, and much of the advantage of low sampling flow is lost. We propose to use a direct sampling method by mass spectrometer that overcomes these deficiencies. METHODS: In the present study, the original high resistance capillary of a QP 9000 mass spectrometer was inserted through the wall of a hyperbaric chamber. Series A: Air and pure nitrogen flowed alternately (1 s each) via the sampling tip of the mass spectrometer. Series B: End expired CO2 from 15 immersed, professional divers exercising at 405 kPa was measured in a screening test for CO2 retention for nitrox diving. RESULTS: There was no difference in the recorded rise time, fall time and plateau reached in the concentration of oxygen at pressures of 101, 202, 303, 405 and 506 kPa. The new sampling method functioned correctly throughout the full-scale experiment, and the recording of end tidal CO2 was more precise than in the conventional method. CONCLUSIONS. Direct sampling of gases from a hyperbaric chamber by the QP 9000 mass spectrometer has many advantages over sampling of the same gases once they are outside the chamber.

PCO(2) threshold for CNS oxygen toxicity in rats in the low range of hyperbaric PO(2).

Central nervous system (CNS) oxygen toxicity, as manifested by the first electrical discharge (FED) in the electroencephalogram, can occur as convulsions and loss of consciousness. CO(2) potentiates this risk by vasodilation and pH reduction. We suggest that CO(2) can produce CNS oxygen toxicity at a PO(2) that does not on its own ultimately cause FED. We searched for the CO(2) threshold that will result in the appearance of FED at a PO(2) between 507 and 253 kPa. Rats were exposed to a PO(2) and an inspired PCO(2) in 1-kPa steps to define the threshold for FED. The results confirmed our assumption that each rat has its own PCO(2) threshold, any PCO(2) above which will cause FED but below which no FED will occur. As PO(2) decreased from 507 to 456, 405, and 355 kPa, the percentage of rats that exhibited FED without the addition of CO(2) (F(0)) dropped from 91 to 62, to 8 and 0%, respectively. The percentage of rats (F) having FED as a function of PCO(2) was sigmoid in shape and displaced toward high PCO(2) with the reduction in PO(2). The following formula is suggested to express risk as a function of PCO(2) and PO(2) [abstract: see text] where P(50) is the PCO(2)for the half response and N is power. A small increase in PCO(2) at a PO(2) that does not cause CNS oxygen toxicity may shift an entire population into the risk zone. Closed-circuit divers who are CO(2)retainers or divers who have elevated inspired CO(2)are at increased risk of CNS oxygen toxicity.