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We investigated 105 professional divers using a computerized visual discrimination trial (Cognitrone) to measure the effects of ambient pressure on reaction times. The possible improvement in performance due to practice was anticipated, and the trials were carried out four times prior to pressurization in a hyperbaric chamber. The effect of increased ambient pressure was measured at 6.0 and 1.9 atm abs, and the potential for residual effects was tested after decompression. The results of our study indicate that repeated testing had a systematic influence on the measured time values. The effects of learning, which were independent of diver age, may have independently influenced response times. Exposure to 6.0 atm abs modified the systematic pattern of learning and was associated with increased reaction times. There were also age-related differences in response times associated with exposure to increased ambient pressures. Younger divers were more susceptible to elevated ambient pressure, evidenced by increased response times at 6 atm abs relative to their older colleagues. One out of every four of the younger divers could be considered susceptible to inert gas narcosis (ION) when an increase of one standard deviation/1SD (19%) or more in discrimination reaction time is used as an indicator. ION susceptibility appears independent of body composition and physical fitness. The slowed response speed experienced at 6.0 atm abs was of short duration and returned to baseline immediately with decompression. Our results suggest that IGN is demonstrated by an impaired learning process and decreased response speed and that some younger divers appear more susceptible.

The interaction of subjective experiences and objective measures of neuropsychological performance during hyperbaric exposure has received less attention in the literature, in part due to the shortage of available and appropriately standardized measures.This study aimed to describe the psychometric properties of a modified version of the Subjective High Assessment Scale when used in the hyperbaric context, by exploring internal reliability, factor structure, associations with psychological variables and simple cognitive delayed recall, and the effect of task focus on the recall of subjective experience.Seventy qualified divers completed dry hyperbaric chamber dives to 607.95 kPa, and completed ratings of their subjective experiences. Some also completed a delayed recall task and psychological measures prior to their dives.The scale displayed good internal consistency, with four meaningful factors emerging. It showed some significant but small associations with trait anxiety and transient mood states, and a small to moderate correlation with recall performance. There was no significant effect of task focus on self-report of subjective experiences.The modified scale, renamed the Subjective Narcosis Assessment Scale here, has useful psychometric properties, and promising potential for future use.

Previous research has consistently demonstrated that inert gas (nitrogen) narcosis affects free recall but not recognition memory in the depth range of 30 to 50 meters of sea water (msw), possibly as a result of narcosis preventing processing when learned material is encoded. The aim of the current research was to test this hypothesis by applying a levels of processing approach to the measurement of free recall under narcosis. Experiment 1 investigated the effect of depth (0-2 msw vs. 37-39 msw) and level of processing (shallow vs. deep) on free recall memory performance in 67 divers. When age was included as a covariate, recall was significantly worse in deep water (i.e., under narcosis), compared to shallow water, and was significantly higher in the deep processing compared to shallow processing conditions in both depth conditions. Experiment 2 demonstrated that this effect was not simply due to the different underwater environments used for the depth conditions in Experiment 1. It was concluded memory performance can be altered by processing under narcosis and supports the contention that narcosis affects the encoding stage of memory as opposed to self-guided search (retrieval).

We investigated the effect of narcosis induced by subanesthetic concentrations of nitrous oxide (N2O), a behavioral analogue for hyperbaric nitrogen, on psychomotor performance. In particular, we assessed individual susceptibility to narcosis.The participants were 12 female and 12 male undergraduate students. Psychomotor assessment was conducted with a computerized Visual Simple Reaction Time (VSRT) test, and Trail Making Tests Part A (TMTA) and Part B (TMT-B). The tests were conducted on two separate occasions in the following order: VSRT, TMT-A, TMT-B. On the first occasion participants conducted the tests breathing room air (air trial), and during the second test they conducted the tests while breathing a normoxic mixture containing 30% N2O (N2O trial).Males had significantly (p = 0.036) shorter VSRT in the air trials. There was no effect of gender on psychomotor performance in the N2O trials. Overall, mean performance in the N2O trials degraded significantly (p = 0.004) only in VSRT. Performance of individual participants exhibited different and inconsistent direction of change in the N2O trials.N2O-induced alterations in psychomotor function are primarily dependent on individual susceptibility to narcosis (i.e., concentration threshold).

The effect of an increased nitrogen partial pressure under hyperbaric conditions is known as nitrogen narcosis (NN). At an ambient pressure of about 4 bar, reduced cognitive performance as well as euphoric effects are reported. We examined the effect of NN on pain perception. 22 subjects completed an experimental (50 meters = 6 bar) and a simulated control dive (0 m = 1 bar) in a hyperbaric chamber. Before and during each dive a standardized cold pressure test was performed. The intensity of pain perceived was assessed with the help of a visual analogue scale; additionally, subjects assessed the subjective effect of NN. The study showed that the perceived pain intensity is significantly reduced under nitrogen narcosis conditions (F1.21 = 5.167, p0.034) when compared to the perceived pain intensity under the control dive conditions (F1.21 = 0.836, p = 0.371). A connection between perceived pain intensity and subjects experience of the NN was not found under the experimental dive condition (r = 0.287, p = 0.195). We could show that even relatively moderate hyperbaric conditions may have an influence on the perception of pain. The results are highly relevant since nitrogen narcosis occurs in divers as well as in medical personnel or construction workers, working under hyperbaric conditions.

Nitrogen (N2) narcosis could interfere with deep submarine escapes, particularly in the escape trunk, where simple but essential tasks are required in order to leave the submarine and start rapid ascent. In a previous study, we had suggested that prolongation of lungs-to-brain circulation time (LBct) may have a protective effect on N2 narcosis, a hypothesis tested in the present study.Computer software was designed to assess the effects of changes in circulation times on N2 uptake and distribution during the extremely rapid pressure changes typical of submarine escapes. Simulations of escapes from 600 to 1,000 fsw (with 200-fsw steps) were performed, with varying dwell times (DT) in the escape trunk (from 10 to 60 seconds, in 10-second steps). Baseline cardiac output (CO) was set at 5 liters/minute, and it was varied through changes in heart rate from 50% to 200% in the escape simulations. LBct was assumed to vary inversely with CO.The risk of N2 narcosis was expressed as equivalent narcosis depth (END) in fsw, corresponding to N2 pressure in the brain after five minutes of air diving at that equivalent depth. The effects of changing CO on the highest END values (corresponding to the peak N2 pressures) reached while in the escape trunk or during entire escapes were tabulated. Depths at which peak N2 occurred were also analyzed. Prolonging LBct appeared to have two advantageous effects: 1. It reduced peak N2 reached both in the escape trunk and during the entire course of the escape 2. It delayed peak N2 to later stages of escapes (i.e., closer to the surface during ascent). These effects were more evident at greater escape depths and with longer DTs.Prolongation of LBct could protect against N2 narcosis and it could plausibly be achieved with the oral administration of a beta-blocker, such as propranolol, prior to deep submarine escape. Animal experiments should be conducted to validate this pharmacological approach.

Nitrogen narcosis occurs in humans at around 0.4 MPa (4 ATA). Hydrogen narcosis occurs between 2.6 and 3.0 MPa. In rats, nitrogen disturbances occur from 1 MPa and a loss of righting reflex around 4 MPa. Neurochemical studies in striatum of rats with nitrogen at 3 MPa (75% of anesthesia threshold) with differential pulse voltammetry have demonstrated a decrease in dopamine (DA) release by neurons originated from the substantia nigra pars compacta (SNc). Such a decrease is found also with compressed argon, which is more narcotic than nitrogen and with the anesthetic gas nitrous oxide. Inversely, compressed helium with its very low narcotic potency induces DA increase. Microdialysis studies in the striatum have indicated that nitrogen also induces a decrease of glutamate concentration. Nitrogen pressure did not modify NMDA glutamate receptor activities in SNc or striatum but enhanced GABAA receptors activities in SNc. Repetitive exposures to nitrogen narcosis suppressed the DA decrease and induced an increase. This fact and the lack of improvement of motor disturbances did not support the hypothesis of a physiological adaptation. The desensitization of the GABAA receptors on DA cells during recurrent exposures and the parallel long-lasting decrease of glutamate coupled to the increase in NMDA receptor sensitivity suggest a nitrogen neurotoxicity or addiction induced by recurrent exposures. The differential changes produced by inert gases indifferent neurotransmitter receptors would support the binding protein theory.

In this study, we investigated the influence of mild narcosis on temperature perception, thermal comfort, and behavioral temperature regulation in humans. Twelve subjects (six males and six females) participated in two trials, during which they wore a water-perfused suit (WPS). The temperature of the WPS (TWPS) fluctuated sinusoidally from 27 degrees to 42 degrees C, at a heating and cooling rate of 1.2 degrees C x min(-1). In the first trial, the subjects had no control over TWPS: They determined their thermal comfort zone (TCZ) by providing a subjective response whenever they perceived the temperature changing from a comfortable to an uncomfortable level and vice versa; in addition, they provided subjective ratings of temperature perception and thermal comfort on a 7-point and 4-point scale, respectively, at each 3 degrees C change in TWPS. In the second trial, subjects could change the direction of TWPS whenever it became uncomfortable by depressing a button on a manual control. The protocols were conducted with subjects breathing either room air (AIR), or a normoxic breathing mixture containing 30% N2O. Subjects perceived increasing TWPS as equally warm and the decreasing TWPS as equally cold with AIR or N2O. However, equal changes in TWPS were perceived as significantly less discomforting (P0.05) during N2O, and the magnitude of the TCZ significantly (P0.01) increased. Thus, narcosis did not alter thermal sensation, but it significantly changed the perception of comfort. These changes were not reflected in the behavioral response. Subjects produced similar TWPS damped-oscillation patterns in the AIR and N2O trials. We conclude that the narcosis-induced alteration in the perception of thermal comfort does not change the preferred temperature, or the ability to behaviorally maintain thermal comfort.

The U.S. Navy recommends submarine escape for depths down to 600 fsw, with deeper escapes entailing the risks of decompression sickness, nitrogen (N2) narcosis and CNS oxygen (O2) toxicity. However, the escape equipment, including the submarine escape and immersion equipment and the escape trunk, could probably function even at 1,000 fsw. Here we report a theoretical analysis of the risks of both N2 narcosis and CNS O2 toxicity for different escape profiles from 600 to 1,000 fsw. The effect of N2 narcosis, calculated as a function of N2 pressure in the brain using Gas Man software, was expressed as equivalent narcosis depth (END), corresponding to the depth at which the same pressure of N2 would be produced in the brain after five minutes of scuba diving with air. The risk of O2-induced convulsions was estimated using the model developed by Arieli et al. Different dwell times (DTs) at maximal pressure in the escape trunk (from 0 to 60 s) and lungs-to-brain circulation times (10 to 30 s) were included in our analysis. When DT in the escape trunk is very short (e.g., 10 s), the risk of either incapacitating N2 narcosis and/or O2-induced convulsions occurring in the trunk is low, even during escapes from 1,000 fsw.

Previous research has demonstrated that nitrogen narcosis causes decrements in memory performance but the precise aspect of memory impaired is not clear in the literature.The present research investigated the effect of narcosis on free recall and recognition memory by appling signal detection theory (SDT) to the analysis of the recognition data.Using a repeated measures design, the free recall and recognition memory of 20 divers was tested in four learning-recall conditions: shallow-shallow (SS), deep-deep (DD), shallow-deep (SD) and deep-shallow (DS). The data was collected in the ocean offDahab, Egypt with shallow water representing a depth of 0-10m (33ft) and deep water 37-40m (121-131ft). The presence of narcosis was independently indexed with subjective ratings.In comparison to the SS condition there was a clear impairment of free recall in the DD and DS conditions, but not the SD condition. Recognition memory remained unaffected by narcosis.It was concluded narcosis-induced memory decrements cannot be explained as simply an impairment of input into long term memory or of self-guided search and it is suggested instead that narcosis acts to reduce the level of processing/encoding of information.

There is a widespread assumption that nitrogen narcosis is comparable to alcohol intoxication, a similarity that may extend to patterns of tolerance. It has been suggested this indicates evidence of a shared biological mechanism but there is a paucity of experimental data to support these claims.The current study aimed to test this assumption by comparing subjective (ratings) and behavioural (Digit Letter Substitution Test) responses to nitrogen narcosis and alcohol.Experiment 1 compared responses to narcosis in 39 participants posited to differ in tolerance based on prior exposure to alcohol (heavy/light drinkers) and narcosis (novice/experienced divers). Experiment 2 compared responses to narcosis and after a 0.5 g/kg dose of alcohol in 23 participants. In both experiments narcosis was measured at depths between 40 and 45m in the ocean off Port Vila, Vanuatu.Experiment 1 measured a significant decrement in the behavioural measure underwater, compared to baseline but failed to find any differential responding to narcosis between drinker or diving experience groups. In contrast, Experiment 2 found positive correlations between alcohol and narcosis on both subjective and behavioural measures, indicating those affected to a greater degree by alcohol were also affected to a greater degree by narcosis.These results support the contention of a relationship between nitrogen narcosis and alcohol, although the role of diving and drinking history, if any, remains obscure.

Nitrogen at pressure produces a neurological syndrome called nitrogen narcosis. Neurochemical experiments indicated that a single exposure to 3 MPa of nitrogen reduced the concentration of dopamine by 20% in the striatum, a structure involved in the control of extrapyramidal motor activity. This effect of nitrogen was explained by enhanced GABAergic neurotransmission through GABAA receptors and, to a lesser extent, by a decreased glutamatergic input to DA cells through NMDA receptors. The aim of this study was to study, under normobaric conditions, possible alterations of NMDA receptor activity in the substantia nigra pars compacta (SNc) induced by repetitive exposures to nitrogen pressure. Under general anesthesia, male Sprague-Dawley rats were implanted in the striatum with multifiber carbon dopamine-sensitive electrodes and in the SNc with guide cannulae for drug injections. After recovery from surgery, the striatal dopamine level was recorded by voltammetry in freely-moving rats, in normobaric conditions, before and after 5 repetitive exposures to 1MPa of nitrogen (threshold of nitrogen narcosis occurrence in rat). The effect of NMDA receptor activity on DA concentration was investigated using agonist (NMDA) and specific antagonist (AP7) SNc administration. Following repetitive nitrogen exposures, the ability of NMDA to elevate DA concentrations was enhanced. In contrast, after nitrogen exposure AP7 produced a paradoxical increase in DA concentration compared to its inhibitory effect before any exposure. Similar responses were obtained after a single exposure to 3MPa nitrogen. Thus, repetitive exposures to nitrogen narcosis produced a sensitization of postsynaptic NMDA receptors on DA cells, related to a decreased glutamatergic input in SNc. Consequently, successive nitrogen narcosis exposures disrupted ion-channel receptor activity revealing a persistent nitrogen-induced neurochemical change underlying the pathologic process.

Hyperbaric nitrogen-oxygen exposure developed in rats a decrement of the striatal dopamine release, which was reversed by repetitive exposures. This dopamine decrease could be the result of the antagonistic effect of nitrogen on NMDA receptors. The increment of the dopamine release, following repetitive exposures to nitrogen, could be attributed to a desensitisation of NMDA receptors to the effects of nitrogen. To test these hypotheses, male Sprague-Dawley rats were implanted with electrodes in the striatum to measure dopamine release by voltammetry and cannula in the substantia nigra pars compacta for NMDA injection. Free-moving rats were exposed up to 3MPa of nitrogen-oxygen mixture before and after 5 exposures to 1MPa. At the first exposure to 3MPa, the dopamine level decreased (-15%) but is counteracted by NMDA administration. In contrast, after repetitive exposure, the second exposure to 3MPa, induces a 10% dopamine increase. NMDA administration significantly potentiated this increase. Our results neither support the hypothesis of an antagonist effect of nitrogen on NMDA receptors at the first exposure, nor that of a NMDA receptor desensitization following repetitive exposures to hyperbaric nitrogen.

Nitrogen at high pressures and anesthetics increase lipid monolayer surface pressure and in turn modulates monolayer associated lipolytic enzyme activity that could alter membrane lipids. We tested the hypothesis that nitrogen at pressures of 5 and 10 megapascals (MPa) and pentobarbital induce alterations in synaptosomal membrane phospholipid and free fatty acid (FFA). Rat cortical synaptosomes in Krebs-Henseleit buffer were placed in steel chambers and incubated for four hours at 37 degrees C: at 5 or 10 MPa of O2/balance N2; at one 0.1 MPa on room air, and with 10 mg pentobarbital. Free fatty acids (FFA) were quantified by thin-layer and gas chromatography, and neutral and acidic lipids by high-pressure thin layer chromatography and protein by Biorad colorimetric assay. Statistical analyses were by ANOVA and posthoc analysis by Neuman-Keuls and Kruskal-Wallis tests at p0.05. Sphyngomyelin, phosphatidylcholine, phosphatidylethanolamine, cerebroside and cholesterol were unchanged by 5 and 10 MPa nitrogen and pentobarbital. Free fatty acids (16:00, 18:00, 18:01, 20:00, 22:0, 22:01 and 24:01) at 10 MPa were reduced compared to 5 MPa (p0.05) but unaffected by pentobarbital. The decrease in synaptosomal membrane FFA at 10 MPa suggests attenuated hydrolysis of membrane phospholipids without detectable alterations in membrane phospholipid composition.

Brain auditory evoked potential (BAEP) in mice exposed to hyperbaric H2O2 pressure was monitored to reveal the correlation between altered synaptic transmission and hydrogen narcosis or isobaric HPNS. Inter peak latencies and wave amplitudes were selected as indices of assessment. The animals were exposed either to He-O2 or H2-O2 at 2.1 MPa and 4.1 MPa. Results showed that synaptic transmission was inhibited to various extents. The inhibition was partly due to the narcotic effect of hydrogen, which was added to the effect caused by hydrostatic pressure. On the other hand, asymmetrical reaction of each segment in the neuro-network might be responsible for the occurrence of HPNS.

The depths from 10 to 30 m are usually not considered narcotic in scuba air-diving, and evidence of psychomotor disturbances attributable to nitrogen narcosis at these depths is weak and contradictory. 15 experienced male divers were tested in a chamber at 1, 2, 3, and 4 bars over five consecutive days using a battery of computer generated psychological tests-Computerized Reactionmeter Drenovac (CRD-series). Total test solving time, minimal single task solving time, total "ballast" time, and total number of errors were recorded. Nitrogen narcosis effects were evident at all hyperbaric pressures with marked performance differences among subjects. MANOVA revealed significant effects of nitrogen partial pressure for groups of the same variables as follows: total test solving time (p0.001), total "ballast" time (p0.001), and total number of errors (p = 0.038), but not for minimal single task solving time. ANOVA showed significant effects of pressure only on tests of visual discrimination of signal location (total test solving time: p = 0.012, total "ballast" time: p0.001), simple convergent visual orientation (total test solving time: p = 0.012), and convergent thinking (total test solving time: p = 0.002, total number of errors: p = 0.049). The order of the pressure exposures had no influence on subject performance. Impaired psychomotor processing found during air exposures from 2 to 4 bars suggests that nitrogen narcosis at depths usually considered safe from its effects might be a problem in underwater operations that require accuracy, speed, limited time of performance, and complex psychomotor skills.

We hypothesized that light-to-moderate inert gas narcosis might play a role in bradycardia in divers by altering sensitivity or response dynamics of arterial baroreflexes. Carotid-cardiac and carotid-mean arterial pressure (MAP) baroreflex response curves were generated by applying multiple levels of neck pressure and suction. Seven healthy volunteers were studied during air breathing (control) and during inhalation of 39% nitrous oxide (N2O). Baseline (pre-stimulus) heart rate (HR) and MAP were not altered by N2O. Range, threshold level, saturation level, and delay of responses did not differ between conditions. For hypertensive stimuli, sensitivity of responses did not differ between air control and N2O inhalation, but for hypotensive stimuli, maximal response gain for HR tended to be reduced with N2O inhalation (P = 0.054). Our results speak against inert gas narcosis as a primary mechanism for hyperbaric bradycardia, but it remains possible that an attenuation of tachycardic responses to hypotensive stimuli plays a role.

Allergic rhinitis and mild respiratory infections have been widely accepted as temporary contraindications for fitness to dive. Nonetheless, several sport and professional divers use antihistamines to ease ear, nose, and throat (ENT) problems, especially for opening tubal ostium. Some divers know they are unfit to dive, but for a variety of reasons (e.g., money or short holiday) they try to clear their ears. Thus, the use of antihistaminic drugs (like clemastine fumarate) is common during diving. This double-blind, crossover study indicates that this special antihistamine does not increase the sedative effects of nitrogen narcosis, nor does it increase the level of cardiac arrhythmias. Liberal use of antihistamines while diving cannot be recommended because of possible complications connected with different preparations and the temporary limitations they impose on the diver.

We investigated adaptation to nitrogen narcosis by compressing 11 highly experienced divers in a hyperbaric chamber to the equivalent of 54.6 meters of seawater once a day for 5 consecutive days. The behavioral component of narcosis was assessed with a serial choice-reaction time (RT) task, and the subjective component with a global magnitude estimate. Supplementary magnitude estimates were obtained with adjectives describing work effectiveness and body sensations. The results showed that there was no adaptation on the RT task, although learning was evident. In contrast, the global estimate dissociated from RT and showed clear adaptation by Day 3. The work effectiveness adjectives followed RT and did not show adaptation. Some body sensation adjectives showed clear adaptation, but others did not. These results lead to the conclusion that the anecdotal reports of adaptation by divers can probably be attributed to the subjective rather than the behavioral component of narcosis. Dissociation of these components suggests mediation by different brain mechanisms, and it is speculated that the gamma-aminobutyric acidA/benzodiazepine receptor complex, which has been implicated in both the anesthetic and anxiolytic properties of agents such as nitrous oxide, may be involved.

It is known that inert gas narcosis slows both reaction time (RT) and the event-related brain potential P300 in a correlated and dose-dependent manner. On the assumption that P300 reflects the time to evaluate a stimulus and RT reflects this time plus the time to select and execute a response, these results have been taken to indicate that the locus of the slowing produced by narcosis is early and influences stimulus evaluation processes. If this is the case, RT and P300 should be slowed identically when cognitive workload is manipulated. To test this prediction, subjects breathed 35% nitrous oxide and responded to differences in the intensity of either visual (Exp. 1, n = 8) or auditory (Exp. 2, n = 10) two-choice oddball stimuli with accuracy controlled at a high level. In both experiments narcosis slowed RT and P300 additively by increasing the intercept rather than the slope of the workload function, but these two measures diverged in one important respect; RT was slowed more than P300, as indicated by an RT-P300 difference analysis. It is concluded that, contrary to previous assumptions, narcosis produces two sources of slowing; one stimulus-related and indexed by P300 and the other response-related and indexed by the RT-P300 difference. Possible mechanisms underlying these sources are discussed.