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Divers commonly breathe air, containing nitrogen. Nitrogen under hyperbaric conditions is a narcotic gas. In dives beyond a notional threshold of 30 m depth (405 kPa) this can cause cognitive impairment, culminating in accidents due to poor decision making. Helium is known to have no narcotic effect. This study explored potential approaches to developing an electroencephalogram (EEG) functional connectivity metric to measure narcosis produced by nitrogen at hyperbaric pressures. Twelve human participants (five female) breathed air and heliox (in random order) at 284 and 608 kPa while recording 32-channel EEG and psychometric function. The degree of spatial functional connectivity, estimated using mutual information, was summarized with global efficiency. Air-breathing at 608 kPa (experienced as mild narcosis) caused a 35% increase in global efficiency compared to surface air-breathing (mean increase = 0.17, 95% CI [0.09-0.25], p = 0.001). Air-breathing at 284 kPa trended in a similar direction. Functional connectivity was modestly associated with psychometric impairment (mixed-effects model r

Introduction: Cold water imposes many risks to the diver. These risks include decompression illness, physical and cognitive impairment, and hypothermia. Cognitive impairment can be estimated using a critical flicker fusion frequency (CFFF) test, but this method has only been used in a few studies conducted in an open water environment. We studied the effect of the cold and a helium-containing mixed breathing gas on the cognition of closed circuit rebreather (CCR) divers. Materials and Methods: Twenty-three divers performed an identical dive with controlled trimix gas with a CCR device in an ice-covered quarry. They assessed their thermal comfort at four time points during the dive. In addition, their skin temperature was measured at 5-min intervals throughout the dive. The divers performed the CFFF test before the dive, at target depth, and after the dive. Results: A statistically significant increase of 111.7% in CFFF values was recorded during the dive compared to the pre-dive values (p < 0.0001). The values returned to the baseline after surfacing. There was a significant drop in the divers’ skin temperature of 0.48°C every 10 min during the dive (p < 0.001). The divers’ subjectively assessed thermal comfort also decreased during the dive (p = 0.01). Conclusion: Our findings showed that neither extreme cold water nor helium-containing mixed breathing gas had any influence on the general CFFF profile described in the previous studies from warmer water and where divers used other breathing gases. We hypothesize that cold-water diving and helium-containing breathing gases do not in these diving conditions cause clinically relevant cerebral impairment. Therefore, we conclude that CCR diving in these conditions is safe from the perspective of alertness and cognitive performance. publishedVersion

Underwater divers are susceptible to neurological risks due to their exposure to increased pressure. Absorption of elevated partial pressure of inert gases such as helium and nitrogen may lead to nitrogen narcosis. Although the symptoms of nitrogen narcosis are known, the molecular mechanisms underlying these symptoms have not been elucidated. Here, we examined the behaviour of the soil nematode Caenorhabditis elegans under scuba diving conditions. We analysed wild-type animals and mutants in the dopamine pathway under hyperbaric conditions, using several gas compositions and under varying pressure levels. We found that the animals changed their speed on a flat bacterial surface in response to pressure in a biphasic mode that depended on dopamine. Dopamine-deficient cat-2 mutant animals did not exhibit a biphasic response in high pressure, while the extracellular accumulation of dopamine in dat-1 mutant animals mildly influenced this response. Our data demonstrate that in C. elegans , similarly to mammalian systems, dopamine signalling is involved in the response to high pressure. This study establishes C. elegans as a powerful system to elucidate the molecular mechanisms that underly nitrogen toxicity in response to high pressure.

INTRODUCTION: When humans breathe compressed air or N(2)-O(2) mixtures at three to four atmospheres pressure, they will experience nitrogen narcosis that may possibly lead to a diving accident, but the underlying mechanisms remain unclear. METHODS: Mice were exposed to 1.6 MPa breathing a N(2)-O(2) mixture adjusted to deliver an inspired PO(2) of 32–42 kPa. The electroencephalogram (EEG) and forced swimming test were used to evaluate the narcotic effect of nitrogen. Neuronal activity was observed via c-Fos expression in cortex and hippocampus tissue after decompressing to the surface. To further investigate underlying molecular mechanisms, we incubated cultured hippocampal neurons with various NMDA concentrations, and measured expression of NMDA receptors and its down-stream signal with or without 1.6 MPa N(2)-O(2) exposure. RESULTS: Both the frequency of the EEG and the drowning time using the forced swimming test were significantly decreased during exposure to 1.6 MPa N(2)-O(2) (P < 0.001). Additionally, in cultured hippocampal neurons, the increased levels of phosphorylated NR2B and cAMP-response element binding protein (CREB) induced by NMDA stimulation were significantly inhibited by exposure to 1.6 MPa N(2)-O(2). CONCLUSION: Our findings indicated that NR2B-containing NMDA receptors were inhibited during nitrogen narcosis.

Divers try to limit risks associated with their sport, for instance by breathing enriched air nitrox (EANx) instead of air. This double blinded, randomized trial was designed to see if the use of EANx could effectively improve cognitive performance while diving., info:eu-repo/semantics/published

Introduction Gas narcosis impairs divers when diving deeper. Pupillometry is sensitive to alcohol intoxication and it has been used in anaesthesia to assess nitrous oxide narcosis. It is a potential novel method to quantify narcosis in diving. The aim of this study was to evaluate pupillometry for objective measurement of narcosis during exposure to hyperbaric air or nitrous oxide. Method Pupil size in 16 subjects was recorded directly at surface pressure and during air breathing at 608 kPa (equivalent to 50 metres' seawater depth) in a hyperbaric chamber. Another 12 subjects were exposed to nitrous oxide at end-tidal percentages of 20, 30 and 40% in random order at surface pressure. Pupil size and pupil light reflex were recorded at baseline and at each level of nitrous oxide exposure. Results Pupil size did not significantly change during exposure to hyperbaric air or nitrous oxide. The pupil light reflex, evaluated using percentage constriction and minimum diameter after exposure to a light stimulus, was affected significantly only during the highest nitrous oxide exposure - an end-tidal level of 40%. Conclusion Pupillometry is insensitive to the narcotic effect of air at 608 kPa in the dry hyperbaric environment and to the effects of low dose nitrous oxide. Pupillometry is not suitable as a monitoring method for gas narcosis in diving.

Cognitive impairment related to inert gas narcosis (IGN) is a threat to diving safety and operations at depth that might be reduced by using enriched air nitrox (EANx) mixtures. Using critical flicker fusion frequency (CFFF), a possible early detection of cognitive abilities/cerebral arousal impairment when breathing different oxygen (O2) fractions was investigated., SCOPUS: ar.j, info:eu-repo/semantics/published

Underwater divers face several potential neurological hazards when breathing compressed gas mixtures including nitrogen narcosis which can impact diver's safety. Various human studies have clearly demonstrated brain impairment due to nitrogen narcosis in divers at 4 ATA using critical flicker fusion frequency (CFFF) as a cortical performance indicator. However, recently some authors have proposed a probable adaptive phenomenon during repetitive exposure to high nitrogen pressure in rats, where they found a reversal effect on dopamine release., info:eu-repo/semantics/published

Gases that are not metabolized by the organism are thus chemically inactive under normal conditions. Such gases include the "noble gases" of the Periodic Table as well as hydrogen and nitrogen. At increasing pressure, nitrogen induces narcosis at 4 absolute atmospheres (ATAs) and more in humans and at 11 ATA and more in rats. Electrophysiological and neuropharmacological studies suggest that the striatum is a target of nitrogen narcosis. Glutamate and dopamine release from the striatum in rats are decreased by exposure to nitrogen at a pressure of 31 ATA (75% of the anesthetic threshold). Striatal dopamine levels decrease during exposure to compressed argon, an inert gas more narcotic than nitrogen, or to nitrous oxide, an anesthetic gas. Inversely, striatal dopamine levels increase during exposure to compressed helium, an inert gas with a very low narcotic potency. Exposure to nitrogen at high pressure does not change N-methyl-d-aspartate (NMDA) glutamate receptor activities in Substantia Nigra compacta and striatum but enhances gama amino butyric acidA (GABAA) receptor activities in Substantia Nigra compacta. The decrease in striatal dopamine levels in response to hyperbaric nitrogen exposure is suppressed by recurrent exposure to nitrogen narcosis, and dopamine levels increase after four or five exposures. This change, the lack of improvement of motor disturbances, the desensitization of GABAA receptors on dopamine cells during recurrent exposures and the long-lasting decrease of glutamate coupled with the higher sensitivity of NMDA receptors, suggest a nitrogen toxicity induced by repetitive exposures to narcosis. These differential changes in different neurotransmitter receptors would support the binding protein theory. © 2016 American Physiological Society. Compr Physiol 6:1579-1590, 2016.

Human beings are exposed to compressed air or a nitrogen-oxygen mixture, they will produce signs and symptoms of nitrogen narcosis such as amnesia or even loss of memory, which may be disappeared once back to the normobaric environment. This study was designed to investigate the effect of nitrogen narcosis induced by repetitive hyperbaric nitrogen-oxygen mixture exposure on long-term cognitive function in newborn mice and the underlying mechanisms. The electroencephalogram frequency was decreased while the amplitude was increased in a pressure-dependent manner during 0.6, 1.2, 1.8 MPa (million pascal) nitrogen-oxygen mixture exposures in adult mice. Nitrogen narcosis in postnatal days 7-9 mice but not in adult mice induced by repetitive hyperbaric exposure prolonged the latency to find the platform and decreased the number of platform-site crossovers during Morris water maze tests, and reduced the time in the center during the open field tests. An increase in the expression of cleaved caspase-3 in the hippocampus and cortex were observed immediately on the first day after hyperbaric exposure, and this lasted for seven days. Additionally, nitrogen narcosis induced loss of the dendritic spines but not of the neurons, which may mainly account for the cognitive dysfunction. Nitrogen narcosis induced long-term cognitive and emotional dysfunction in the postnatal mice but not in the adult mice, which may result from neuronal apoptosis and especially reduction of dendritic spines of neurons.

BACKGROUND Nitrogen (N2) in air causes cognitive impairment from gas narcosis when breathed at increased ambient pressures. This impairment might be reduced by using enriched air nitrox (EANx) mixtures, which have a higher oxygen and lower N2 content compared to air. This study aimed to investigate if divers differed in memory ability and self-assessment when breathing air and EANx30. METHODS The effect of depth (shallow vs. deep) and breathing gas (air vs. EANx30) on memory ability and subjective ratings of impairment was compared in 20 divers. RESULTS Memory performance was significantly worse in deep water (Air: M = 22.1%, SD = 21.7%; EANx30: M = 22.1%, SD = 17.2%) compared to shallow water (Air: M = 29.2%, SD = 18.3%; EANx30: M = 33.3%, SD = 18.2%), but this impairment did not differ significantly between air and EANx30. Subjective ratings of impairment increased significantly from shallow water (Air: M = 5.2, SD = 5.9; EANx30: M = 3.0, SD = 4.4) to deep water (Air: M = 36.8, SD = 25.3; EANx30: M = 24.8, SD = 16.1) when breathing both air and EANx30. However, ratings were significantly lower when breathing EANx30 compared to air when in the deep water. DISCUSSION It was concluded EANx30 does not reduce narcotic impairment over air. Additionally, divers were able to make a correct global self-assessment they were impaired by narcosis, but were unable to make a finer assessment, leading them to erroneously believe that EANx30 was less narcotic than air.

Background: This paper considers the relationship between measures of personality and mood states, and susceptibility to inert gas narcosis. It briefly reviews the topics of inert gas narcosis affecting personality, and personality affecting the susceptibility to inert gas narcosis. There appears to be is a theoretical argument for a possible relationship between measures of personality, mood states, and susceptibility to narcosis. Practically, such a relationship may speak to issues in selection, training and preparation, risk assessments, and even accident investigation in the diving and/or hyperbaric environment. Materials and methods: Twenty one divers completed measures of personality and mood states, and were then compressed to 709 kPa (equivalent to 60 msw) in a dry compression chamber, where they completed a task measuring speed of information processing, and a scale measuring subjective narcosis. Results and Conclusions: The main finding was the absence of any significant correlations between measures of personality traits and mood, and susceptibility to inert gas narcosis. Although the study found no evidence of any major relationship, it is presented as a case study to highlight some of the issues and pitfalls involved in such research. The lessons learned — including the careful defining and describing of concepts, and choosing of samples and measurements — are used to discuss some of the methodological and conceptual issues and future directions for researchers to consider.

Previous microdialysis studies performed in rats have revealed a decrease of striatal dopamine and glutamate induced by nitrogen narcosis. We sought to establish the hypothetical role of the glutamatergic corticostriatal pathway because of the glutamate deficiency which occurs in the basal ganglia in this hyperbaric syndrome. Retrodialysis with 1 mM of Saclofen and 100 mM of KCl in the prefrontal cortex under normobaric conditions led to an increase in striatal levels of glutamate by 95.2% and no changes in dopamine levels. Under 3 MPa of nitrogen and with the infusion, the rate of striatal glutamate decreased by 51.3%, to a greater extent than under pressurised nitrogen alone (-23.8%). The rate of dopamine decreased, which also occurred under pressurised nitrogen (-36.9 and -31.4%, respectively). In conclusion, the function of the corticostriatal pathway is affected by nitrogen under pressure. This suggests that the nitrogen-induced break point seems to be located at the glutamatergic striatopetal neurons.

Nervous disorders may occur after an organism is saturated with inert gases, which may alter the lipid bilayer structure, according to their liposolubility coefficient. Increase in the nitrogen partial pressure induces a neurological syndrome called 'nitrogen narcosis'. By contrast, high pressures of helium induce epilepsy, an high-pressure nervous syndrome symptom. On the basis of an analogy with anaesthetic mechanisms, we used TREK-1 knockout mice, earlier described to volatile the anaesthetics resistance. These mice had a higher threshold of resistance to the narcotic effects of nitrogen and to the death after recurrent epileptic seizure induced by high pressure. TREK-1 channels seem to play a key role in modulating the anaesthetic potential of inert gases and in neuroprotection.

Exposure to nitrogen-oxygen mixture at high pressure induces narcosis, which can be considered as a first step toward general anaesthesia. Narcotic potencies of inert gases are attributed to their lipid solubility. Nitrogen narcosis induces cognitive and motor disturbances that occur from 0.3 MPa in man and from 1 MPa in rats. Neurochemical studies performed in rats up to 3 MPa have shown that nitrogen pressure decreases striatal dopamine release like argon, another inert gas, or nitrous oxide, an anaesthetic gas. Striatal dopamine release is under glutamatergic and other amino acid neurotransmission regulations. The aim of this work was to study the effects of nitrogen at 3 MPa on striatal amino acid levels and to compare to those of 3 MPa of helium which is not narcotic at this pressure, by using a new technique of microdialysis samples extraction under hyperbaric conditions, in freely moving rats. Amino acids were analysed by HPLC coupled to fluorimetric detection in order to appreciate glutamate, aspartate, glutamine and asparagine levels. Nitrogen-oxygen mixture exposure at 3 MPa decreased glutamate, glutamine and asparagine concentrations. In contrast, with helium-oxygen mixture, glutamate and aspartate levels were increased during the compression phase but not during the stay at maximal pressure. Comparison between nitrogen and helium highlighted the narcotic effects of nitrogen at pressure. As a matter of fact, nitrogen induces a reduction in glutamate and in other amino acids that could partly explain the decrease in striatal dopamine level as well as the motor and cognitive disturbances reported in nitrogen narcosis.

Nitrogen pressure exposure in rats results in decreased dopamine (DA) release at the striatal terminals of the substantia nigra pars compacta (SNc) dopaminergic neurons, demonstrating the narcotic potency of nitrogen. This effect is attributed to decreased excitatory and increased inhibitory inputs to dopaminergic neurons, involving a change in NMDA and GABA(A) receptor function. We investigated whether repetitive exposures to nitrogen modify the excitatory and inhibitory control of the dopaminergic nigro-striatal pathway. We used voltammetry to measure dopamine levels in freely-moving rats, implanted with dopamine-sensitive electrodes in the striatum. NMDA/GABA(A) receptor agonists (NMDA/muscimol) and antagonists (AP7/gabazine) were administered through a guide-cannula into the SNc, and their effects on striatal dopamine levels were measured under normobaric conditions, before and after five repetitive exposures to 1 MPa nitrogen. NMDA-mediated dopamine release was greater following repetitive exposures, AP7-mediated inhibition of glutamatergic input was blocked, suggesting that NMDA receptor sensitivity was increased and glutamate release reduced. Muscimol did not modify dopamine levels following repetitive exposures, whereas the effect of gabazine was greater after exposures than before. This suggested that interneuronal GABA(A) receptors were desensitized, leading to an increased GABAergic input at dopaminergic cells. Thus, repetitive nitrogen exposure induced persistent changes in glutamatergic and GABAergic control of dopaminergic neurons, resulting in decreased activity of the nigrostriatal pathway.

Exposure to the underwater environment for pleasure or work poses many challenges on the human body including thermal stress, barotraumas, decompression sickness as well as the acute effects of breathing gases under pressure. With the popularity of recreational self-contained underwater breathing apparatus (SCUBA) diving on the increase and deep inland dive sites becoming more accessible, it is important that we understand the effects of breathing pressurised gas at depth can have on the body. One of the common consequences of hyperbaric gas is the narcotic effect of inert gas. Nitrogen (a major component of air) under pressure can impede mental function and physical performance at depths of as little as 10 m underwater. With increased depth, symptoms can worsen to include confusion, disturbed coordination, lack of concentration, hallucinations and unconsciousness. Narcosis has been shown to contribute directly to up to 6% of deaths in divers and is likely to be indirectly associated with other diving incidents at depth. This article explores inert gas narcosis, the effect on divers’ movement and function underwater and the proposed physiological mechanisms. Also discussed are some of the factors that affect the susceptibility of divers to the condition. In conclusion, understanding the cause of this potentially debilitating problem is important to ensure that safe diving practices continue.

Previous studies have demonstrated opposite effects of high-pressure helium and nitrogen on extracellular dopamine (DA) levels, which may reflect disturbances on the synthesis, release or metabolic mechanisms. Intrastriatal microdialysis was used to measure the precursor (tyrosine), DA and its metabolites (DOPAC, HVA) levels under nitrogen- or helium- at pressure up to 3 MPa. Under 3 MPa of helium–oxygen breathing mixtures, the extracellular concentration of tyrosine is decreased while the extracellular concentration of DA is increased. On the contrary, nitrogen–oxygen breathing mixture at the same pressure increased extracellular tyrosine concentration and decreased DA release. Under both conditions, an increment of the DOPAC and HVA levels could be noted. Our results suggest that changes in DA release and metabolism during high-pressure helium exposure reflect the effect of the pressure per se, whereas the intrinsic effects of narcotic gases, although sensitive to pressure, would be revealed by hyperbaric nitrogen exposure.

Inert gas narcosis is a neurological syndrome appearing when humans or animals are exposed to hyperbaric inert gases (nitrogen, argon) composed by motor and cognitive impairments. Inert gas narcosis induces a decrease of the dopamine release at the striatum level, structure involved in the regulation of the extrapyramidal motricity. We have investigated, in freely moving rats exposed to different narcotic conditions, the relationship between the locomotor and motor activity and the striatal dopamine release, using respectively a computerized device that enables a quantitative analysis of this behavioural disturbance and voltammetry. The use of 3 MPa of nitrogen, 2 MPa of argon and 0.1 MPa of nitrous oxide, revealed after a transient phase of hyperactivity, a lower level of the locomotor and motor activity, in relation with the decrease of the striatal dopamine release. It is concluded that the striatal dopamine decrease could be related to the decrease of the locomotor and motor hyperactivity, but that other(s) neurotransmitter(s) could be primarily involved in the behavioural motor disturbances induced by narcotics. This biphasic effect could be of major importance for future pharmacological investigations, and motor categorization, on the basic mechanisms of inert gas at pressure.

Exposure to the undersea environment has unique effects on normal physiology and can result in unique disorders that require an understanding of the effects of pressure and inert gas supersaturation on organ function and knowledge of the appropriate therapies, which can include recompression in a hyperbaric chamber. The effects of Boyle's law result in changes in volume of gas-containing spaces when exposed to the increased pressure underwater. These effects can cause middle ear and sinus injury and lung barotrauma due to lung overexpansion during ascent from depth. Disorders related to diving have unique presentations, and an understanding of the high-pressure environment is needed to properly diagnose and manage these disorders. Breathing compressed air underwater results in increased dissolved inert gas in tissues and organs. On ascent after a diving exposure, the dissolved gas can achieve a supersaturated state and can form gas bubbles in blood and tissues, with resulting tissue and organ damage. Decompression sickness can involve the musculoskeletal system, skin, inner ear, brain, and spinal cord, with characteristic signs and symptoms. Usual therapy is recompression in a hyperbaric chamber following well-established protocols. Many recreational diving candidates seek medical clearance for diving, and healthcare providers must be knowledgeable of the environmental exposure and its effects on physiologic function to properly assess individuals for fitness to dive. This review provides a basis for understanding the diving environment and its accompanying disorders and provides a basis for assessment of fitness for diving.