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PubMed2003

Striatal dopamine release and biphasic pattern of locomotor and motor activity under gas narcosis.

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.

Animals↗

PubMed1993

Relationship between the event-related brain potential P300 and inert gas narcosis.

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.

Adult↗

PubMed1985

Effects of inert gas narcosis on behavior--a critical review.

The effects of inert gas narcosis on behavior before unconsciousness are reviewed with particular attention to four issues. The first is whether the qualitative behavioral effects of all inert gases are identical. Evidence is limited but does not contradict an affirmative answer. This is consistent with the unitary hypothesis of narcosis at the physicochemical level. The second issue concerns the relative merits of four approaches to narcosis; (a) the descriptive model, (b) the hierarchical organization hypothesis, (c) the operant paradigm, and (d) the slowed processing model. It is concluded that the latter two are showing some promise. In particular, operant techniques allow more sophisticated measures of narcosis in animals than behavioral end points, such as loss of the righting reflex. The slowed processing model claims that the majority of performance deficits in humans are caused by a single fundamental deficit, slowing of information processing due to decreased arousal. This slowing is usually accompanied by alterations in task strategy. These alterations, in combination with cumulative slowing in working memory, are said to account for the various manifestations of narcosis on complex tasks. The third issue concerns adaptation to narcosis. There is some evidence that adaptation can occur but it is unclear whether the cause is learning specific to narcosis or development of a physiological tolerance. However, adaptation has not always been found and the variables controlling its presence or absence have yet to be identified. The fourth issue concerns the modifying effects of various factors, such as carbon dioxide and anxiety, on narcosis. Methodological and conceptual problems hinder interpretation of the evidence in this area but, contrary to some current views, there appears to be no conclusive evidence that any factor other than ethanol potentiates narcosis. Some implications of these conclusions for diving operations are discussed.

Amphetamine↗

PubMed1993

Visual/vestibular effects of inert gas narcosis.

Divers breathing compressed air at depths beyond 30 m experience a type of behavioural impairment known as inert gas narcosis. This condition degrades performance on a wide range of tasks and has the potential to compromise safety. Symptoms associated with narcosis include slowed response time, amnesia, and euphoria. Studies have also found disturbances to mechanisms regulating ocular control in response to vestibular stimulation; however, these experiments have been limited to very low frequency head movement (0.2 Hz). Thus, to further examine the effects of narcosis on visual/vestibular mechanisms, the vestibular ocular reflex (VOR) was assessed across a range of higher frequencies more representative of natural head movement (2.0-4.7 Hz). Seven subjects were tested prior to, during and after exposure to narcosis which was induced using 30% nitrous oxide. Standard room air was breathed as a control. The results indicated that narcosis decreased the velocity of compensatory eye movements in response to head rotation (decrease in VOR-gain), with more pronounced decreases occurring at the higher frequencies. The lag between eye and head position (phase lag) was also decreased by nitrous oxide; an effect that was again more pronounced at higher frequencies. These results indicate that narcosis disrupts ocular regulatory mechanisms which help to stabilize images on the retina during head movement.

Adult↗

PubMed1993

Dissociation of the effects of alcohol and amphetamine on inert gas narcosis using reaction time and P300 latency.

Alcohol exacerbates and amphetamine ameliorates the slowing of reaction time (RT) produced by inert gas narcosis. The event-related brain potential P300 was used to determine whether these drug effects involve stimulus- or response-related processes, since P300 largely reflects the time to evaluate a stimulus while RT reflects this time plus the time to select and execute a response. Subjects breathed nitrous oxide (N2O) alone and in combination with ethyl alcohol or dextroamphetamine while responding to visually presented names that differed in probability (the oddball paradigm). N2O slowed P300, but this measure was comparatively insensitive to the exacerbation and amelioration that were indexed by RT. Relative to N2O alone, an RT-P300 difference was found for amphetamine + N2O but not for alcohol + N2O. We conclude that exacerbation involves both stimulus- and response-related processes but amelioration involves only the latter. This pattern of results can be explained by a model in which the drugs modulate slowing via the two energetical dimensions of arousal and activation, which influence stimulus- and response-related processes, respectively.

Action Potentials↗

PubMed1977

Does the evoked response measure inert gas narcosis?

The purpose of this review is to examine the validity of change in the cortical evoked response as a measure of inert gas narcosis in humans. Three criteria are defined which must all be met if a nonbehavioral measure is to be accepted as an indicator of narcosis. The evoked response is assessed in terms of these criteria. Two classes of experiments which have used the evoked response in hyperbaric ocnditions are identified. The first class allows the evoked response to be assessed against more than one of these criteria. The outcome of every experiment in this class supports the view that the evoked response is not a valid measure of narcosis. The second class of experiment assumed that the evoked response is a measure of narcosis and were not designed to assess validity appropriately. Arguments by Kinney and associates in support of the assumption of validity are shown to be unsound. Possible explanations for inability to demonstrate validity are discussed and it is suggested that factors other than narcotic potency of the breathing gas mixture determine or at least play a major role in determining amplitude of the evoked response.

Acoustic Stimulation↗

PubMed1987

Effects of inert gas narcosis on rehearsal strategy in a learning task.

Two experiments were conducted to examine the effects of 35% nitrous oxide (N2O) on rehearsal strategy while learning a list of words in a free-recall paradigm. In experiment 1, the subjects learned the list while rehearsing the words aloud. Learning was slowed and an analysis of the recorded rehearsal protocols revealed a decrease in the overall rate of rehearsal. In addition, there was a decrease in both the number of words rehearsed together and the proportion of words rehearsed from earlier serial positions in the list. In experiment 2, the subjects were required to follow a different rehearsal protocol which was identical for both N2O and the air-breathing control. They had no difficulty following this protocol, but learning was still slowed. These results demonstrate that rehearsal strategies may be modified by narcosis but can be manipulated experimentally. This is consistent with the hypothesis that strategic variables play an important role in the slowed processing model of inert gas narcosis.

Adult↗

PubMed1986

Effects of inert gas narcosis on the vestibular ocular reflex.

A study was conducted to examine the vestibular ocular reflex (VOR) during narcosis. The slow phase velocity of the nystagmus was measured in six subjects by means of electronystagmography during the inhalation of 25% nitrous oxide. It was found that nitrous oxide increased the velocity of the slow phase component of the VOR by approximately 50%. This result indicates that the gain of the VOR is effectively increased during nitrous oxide induced narcosis. It appears that the vestibular end organs and/or the central pathways controlling nystagmus are affected by nitrous oxide and this may be a reason for the disruption in balance associated with inert gas narcosis.

Adult↗

PubMed1969