Central Nervous System Oxygen Toxicity in Closed-Circuit Scuba Divers

Butler, FK; Thalmann, ED

doi:10.21236/ada170879

Cited by 29 publications

(47 citation statements)

References 1 publication

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“…In the rat brain stem slice, however, extreme hypercapnia, which also impairs neuronal excitability, decreases pH i , on average, from 7.24 (5% CO 2 ) to 6.71 (33% CO 2 ) to 6.67 (50% CO 2 ) and to 6.49 (100% CO 2 at PB ϳ1 ATA) in locus coeruleus neurons and results in abnormal electrical activity (56). risk of decompression sickness during and after ascent (36,37). However, breathing pure O 2 or nitrox (Ͼ21% O 2 ) also increases the risk of CNS O 2 toxicity at greater depths (Fig.…”

Section: Co 2 Toxicitymentioning

confidence: 99%

“…If, however, the subject is not removed immediately from the hyperoxic environment, then continued exposure to HBO 2 can result, first, in permanent neurological damage and paralysis (i.e., the "John Bean effect") and eventually death with prolonged exposure (12). Presently, CNS O 2 toxicity is the limiting factor in protocols employed for closed-circuit diving operations by combat divers (37) and for HBOT (38).…”

Section: Co 2 Toxicitymentioning

confidence: 99%

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Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

Dean¹,

Mulkey²,

Garcia³

et al. 2003

Journal of Applied Physiology

175

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III. Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures. J Appl Physiol 95: 883-909, 2003; 10.1152/japplphysiol.00920.2002.-As ambient pressure increases, hydrostatic compression of the central nervous system, combined with increasing levels of inspired PO 2, PCO2, and N2 partial pressure, has deleterious effects on neuronal function, resulting in O 2 toxicity, CO2 toxicity, N2 narcosis, and high-pressure nervous syndrome. The cellular mechanisms responsible for each disorder have been difficult to study by using classic in vitro electrophysiological methods, due to the physical barrier imposed by the sealed pressure chamber and mechanical disturbances during tissue compression. Improved chamber designs and methods have made such experiments feasible in mammalian neurons, especially at ambient pressures Ͻ5 atmospheres absolute (ATA). Here we summarize these methods, the physiologically relevant test pressures, potential research applications, and results of previous research, focusing on the significance of electrophysiological studies at Ͻ5 ATA. Intracellular recordings and tissue PO 2 measurements in slices of rat brain demonstrate how to differentiate the neuronal effects of increased gas pressures from pressure per se. Examples also highlight the use of hyperoxia (Յ3 ATA O 2) as a model for studying the cellular mechanisms of oxidative stress in the mammalian central nervous system. anesthesia; carbon dioxide toxicity; free radicals; high-pressure nervous syndrome; membrane potential; nitrogen narcosis; oxidative stress; oxygen toxicity; polarographic oxygen electrode MOST HUMANS ARE PHYSIOLOGICALLY adapted to live and work near sea level, where ambient pressure is ϳ1 atmosphere absolute (ATA).1 Nonetheless, we exploit a continuum of barometric pressure (PB) ranging from the near vacuum of outer space, which we survive during Space Shuttle extravehicular activity by wearing a 4.3 lb./in.2 absolute (psia) pressure suit (30,300 ft. pressure equivalent, 0.29 ATA) (120, 220), down to the summit of Mt. Everest at 29,029 ft., where PB is 0.31 ATA (221), to ocean depths as great as 2,300 ft. of sea water (fsw), where PB increases to ϳ70 ATA (18). These situations are the pressure extremes of our inhabitable environment, which only relatively few highly trained individuals have ever occupied.Military personnel, medical personnel, and other humans, however, frequently encounter levels of hyperbaric pressure (i.e., Ͼ1 ATA) of lesser degrees in their normal work environments. Examples of moderate hyperbaric environments (e.g., Ͻ5 ATA) include the following: patients and medical attendants undergoing hyperbaric O 2 therapy (HBOT) (38,203); diving with an underwater breathing apparatus for recreational, professional (oil and salvage companies), and combat purposes (89); simulated dry and wet dives for hyperbaric research and dive training (217); and working in the compressed atmosphere of a subterranean environment (117). Abnormal work environments resulting from catastrophic accident...

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Section: Co 2 Toxicitymentioning

confidence: 99%

Section: Co 2 Toxicitymentioning

confidence: 99%

Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

Dean¹,

Mulkey²,

Garcia³

et al. 2003

Journal of Applied Physiology

175

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“…PFT changes: f = reduced peak flow, v = reduced vital capacity, d = reduced diffusing capacity, v1 reduced FEV 1 …”

Section: Divingmentioning

confidence: 99%

“…The current shallow-water exposure limit, four hours breathing oxygen at 25 fsw or less in any 24-hour period, was established somewhat arbitrarily as a known "safe" exposure. 1 It does not represent a tested upper limit before PO 2 T develops. However, when the possibility of doubling the shallow water exposure time was explored, many pulmonary symptoms and measurable pulmonary function deficits were seen after seven to eight hours of breathing oxygen underwater.…”

Section: Introductionmentioning

confidence: 99%

Pulmonary Effects of Submerged Breathing of Air or Oxygen

Shykoff¹

2002

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“…If divers immediately inhale HBO, inert gases dissolved in the body can be displaced and fast-buoyancy ascent escape is conducted; thus, the safety of the crew can be ensured and the condition and sequelae of decompression sickness are reduced. After a great-depth and long-term underwater operation is completed, decompression time is significantly shortened and decompression efficiency is significantly enhanced if HBO is used in decompression [1][2][3]. However, continuous inhalation of high-pressure oxygen can cause central nervous system oxygen toxicity (CNS-OT) [4].…”

Section: Introductionmentioning

confidence: 99%

Glutamate metabolism of astrocytes during hyperbaric oxygen exposure and its effects on central nervous system oxygen toxicity

Chen

Zhongzhuang

et al. 2016

NeuroReport

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Hyperbaric oxygen (HBO) has been used widely in many underwater missions and clinical work. However, exposure to extremely high oxygen pressure may cause central nervous system oxygen toxicity (CNS-OT). The regulation of astrocyte glutamate metabolism is closely related to epilepsy. This study aimed to observe the effects of HBO exposure on glutamate metabolism in astrocytes and confirm the role of glutamate metabolism in CNS-OT. Anesthetized rats were exposed to 5 atmosphere absolute HBO for 80 min and microdialysis samples of brain interstitial fluid were continuously collected. Extracellular glutamate and glutamine concentrations were also detected. Freely moving rats were exposed to HBO of the same pressure for 20 min and glutamine synthetase (GS) activity in brain tissues was measured. Finally, we observed the effects of different doses of drugs related to glutamate metabolism on the latency of CNS-OT. Results showed that HBO exposure significantly increased glutamate content, whereas glutamine content was significantly reduced. Moreover, HBO exposure significantly reduced GS activity. Glutamate transporter-1 (GLT-1) selective antagonist ceftriaxone prolonged CNS-OT latency, whereas GLT-1 selective inhibitor dihydrokainate shortened CNS-OT latency. In summary, HBO exposure improved glutamate concentration and reduced glutamine concentration by inhibition of GS activity. GLT-1 activation also participated in the prevention of HBO-induced CNS-OT. Our research will provide a potential new target to terminate or attenuate CNS-OT.

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Central Nervous System Oxygen Toxicity in Closed-Circuit Scuba Divers

Cited by 29 publications

References 1 publication

Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

Pulmonary Effects of Submerged Breathing of Air or Oxygen

Glutamate metabolism of astrocytes during hyperbaric oxygen exposure and its effects on central nervous system oxygen toxicity

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