Biomedical subjects

Ran Arieli

Publications and source records attributed to Ran Arieli.

9 recordsLinked to original sources

PubMed2006

CNS toxicity in closed-circuit oxygen diving: symptoms reported from 2527 dives.

INTRODUCTION: Oxygen toxicity is a problem in diving and can have fatal consequences in the water. Various aspects of oxygen diving have been studied in dry hyperbaric chambers, but there is a lack of information on in-water diving using closed-circuit oxygen apparatus. METHOD: We collected 2527 dive reports from 473 closed-circuit oxygen divers (a mean of 5.2 reports per diver), and analyzed the relationships between various symptoms and their dependence on depth and diving time. RESULTS: No CNS oxygen toxicity-related symptoms were reported at a depth of 2 m seawater (msw), but their proportion increased at depths from 3 to 6 msw. We found that CNS oxygen toxicity-related symptoms appeared in 2.5% of dives conducted at a Po2 of 119 kPa. The main symptoms and signs reported were headache: 4.5%; nausea: 2.6%; hyperventilation: 2.6%; heavy breathing: 2.4%; dizziness: 1.6%; hiccups: 1.5%; bloody sputum: 1.4%; cold shivering: 1.1%; tinnitus: 0.9%; difficulty maintaining a steady depth: 0.9%; disorientation: 0.6%; tiredness: 0.5%; tingling in the limbs: 0.4%; hearing disturbances: 0.4%; a choking sensation: 0.4%; extreme effort: 0.4%; and loss of consciousness: 0.3%. DISCUSSION: Environmental factors, light vs. dark and temperature, had no effect on symptoms. The number of symptoms increased with diving time. Divers who experienced amnesia, facial twitching, hearing disturbances (p < 0.001), and disorientation (p < 0.014) were prone to suffer loss of consciousness. It was found that some divers are more sensitive to oxygen than others (p < 0.0001).

Airway Obstruction↗

PubMed2004

Response to CO2 in novice closed-circuit apparatus divers and after 1 year of active oxygen diving at shallow depths.

Elevated arterial Pco(2) (hypercapnia) has a major effect on central nervous system oxygen toxicity in diving with a closed-circuit breathing apparatus. The purpose of the present study was to follow up the ability of divers to detect CO(2) and to determine the CO(2) retention trait after 1 year of active oxygen diving with closed-circuit apparatus. Ventilatory and perceptual responses to variations in inspired CO(2) (range: 0-5.6 kPa, 0-42 Torr) during moderate exercise were assessed in Israeli Navy combat divers on active duty. Tests were carried out on 40 divers during the novice oxygen diving phase (ND) and the experienced oxygen diving phase. No significant changes were found between the two phases for the minimal mean inspired Pco(2) that could be detected. The mean (with SD in parentheses) end-tidal Pco(2) during exposure to an inspired Pco(2) of 5.6 kPa (42 Torr) was significantly higher in the novice diving phase than in the experienced diving phase [8.1 kPa (SD 0.7), 62 Torr (SD 5) and 7.8 kPa (SD 0.6), 59 Torr (SD 4), respectively; P < or = 0.001]. One year of shallow oxygen diving activity with a closed-circuit apparatus does not affect the ability to detect CO(2) nor does it lead to increased CO(2) retention; rather, it may even bring about a decrease in this trait. This finding suggests that acquiring experience in oxygen diving with a closed-circuit apparatus at shallow depths does not place the diver at a greater risk of central nervous system oxygen toxicity due to CO(2) retention.

Adult↗

PubMed2004

Hyperbaric oxygen therapy for reduction of secondary brain damage in head injury: an animal model of brain contusion.

Cerebral contusions are one the most frequent traumatic lesions and the most common indication for secondary surgical decompression. The purpose of this study was to investigate the physiology of perilesional secondary brain damage and evaluate the value of hyperbaric oxygen therapy (HBOT) in the treatment of these lesions. Five groups of five Sprague-Dawley rats each were submitted to dynamic cortical deformation (DCD) induced by negative pressure applied to the cortex. Cerebral lesions produced by DCD at the vacuum site proved to be reproducible. The study protocol entailed the following: (1) DCD alone, (2) DCD and HBOT, (3) DCD and post-operative hypoxia and HBOT, (4) DCD, post-operative hypoxia and HBOT, and (5) DCD and normobaric hyperoxia. Animals were sacrificed after 4 days. Histological sections showed localized gross tissue loss in the cortex at injury site, along with hemorrhage. In all cases, the severity of secondary brain damage was assessed by counting the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and caspase 3-positive cells in successive perilesional layers, each 0.5 mm thick. Perilesional TUNEL positive cells suggested the involvement of apoptosis in group 1 (12.24% of positive cells in layer 1). These findings were significantly enhanced by post-operative hypoxia (31.75%, p < 0.001). HBOT significantly reduced the severity and extent of secondary brain damage expressed by the number of TUNEL positive cells in each layer and the volume of the lesion (4.7% and 9% of TUNEL positive cells in layer 1 in groups 2 and 4 respectively, p < 0.0001 and p < 0.003). Normobaric hyperoxia also proved to be beneficial although in a lesser extent. This study demonstrates that the vacuum model of brain injury is a reproducible model of cerebral contusion. The current findings also suggest that HBOT may limit the growth of cerebral contusions and justify further experimental studies.

Animals↗

PubMed2003

Heat acclimation prolongs the time to central nervous system oxygen toxicity in the rat. Possible involvement of HSP72.

Oxygen toxicity of the central nervous system (CNS-OT) can occur during diving with oxygen-enriched gas mixtures, or during hyperbaric medical treatment. CNS-OT is characterised by convulsions and sudden loss of consciousness, which may be fatal in diving. Heat acclimation is known to provide cross-tolerance to various forms of stress in different organs, including the brain. We hypothesised that heat acclimation may delay the onset of CNS-OT in the rat. Male Sprague-Dawley rats were acclimated to an ambient temperature of 32 degrees C for 4 weeks. Rats in the control group were kept at 24 degrees C. Both groups were exposed to oxygen at 608 kPa. EEG was recorded continuously until the appearance of the first electrical discharge preceding clinical convulsions. CO(2) production was measured simultaneously with the EEG. Latency to CNS-OT was measured and brain samples were taken for evaluation of heat shock protein 72 (HSP72) levels by Western blot analysis at the end of the acclimation period and during 4 weeks of deacclimation. Latency to CNS-OT was twice as long in the heat-acclimated rat, with insignificant changes in CO(2) production. This prolongation continued for 2 weeks during deacclimation. There was a significant increase in the level of HSP72 following heat acclimation, with a subsequent decrease during deacclimation. We conclude that heat acclimation prolongs latency to CNS-OT in a way that does not involve changes in metabolic rate. During deacclimation there was a linear relationship between latency to CNS oxygen toxicity and the level of HSP72. A possible beneficial effect of HSP72 is discussed.

Acclimatization↗

PubMed2003

Training improves divers' ability to detect increased CO2.

BACKGROUND: Elevated arterial PCO2 (hypercapnia) is a known risk in diving with closed circuit breathing apparatus. In a retrospective study, we determined CO2 retention and the ability to detect CO2 in novice divers who were either CO2-recognition-trained subjects (TS) or untrained subjects (UTS). METHODS: Ventilatory and perceptual responses to variations in inspired CO2 (range 0-5.6 kPa, 0-42 mm Hg) during moderate exercise were assessed in novice Israeli Navy divers on active duty. Tests were carried out on 231 TS and 213 UTS. RESULTS: The minimal mean inspired PCO2 that could be detected was 4.8 +/- 1.6 kPa (36 +/- 12 mm Hg) in UTS and 2.9 +/- 0.7 kPa (22 +/- 5 mm Hg) in TS (p < 0.0001). No significant changes were found in PETCO2 between the two groups during exposure to a PICO2 of 5.6 kPa (42 mm Hg). There were 46 TS who were found to be CO2 retainers (more than +1 SD above the mean) and 19 were classified as poor detectors (more than +1 SD above the mean). Seven subjects exhibited both traits. During actual oxygen diving performed later by this group, the only four cases of CNS-oxygen toxicity were among those seven subjects (p < 0.01). CONCLUSIONS: We conclude that CO2 recognition training improves the diver's capability to detect CO2. We suggest that a diver who is both a poor CO2 detector and a CO2 retainer will be prone to CNS-oxygen toxicity.

Adult↗

PubMed2003

Model of CNS O2 toxicity in complex dives with varied metabolic rates and inspired CO2 levels.

INTRODUCTION: Clinical hyperbaric oxygen (HBO) therapy and the use of pure oxygen or gases having a high partial pressure of oxygen in diving carry a risk of central nervous system (CNS) oxygen toxicity. Previously, we solved the power equation K = t2(PO2/101.3)C for humans, where t is the exposure time, PO2 is the oxygen pressure, and K is the cumulative oxygen toxicity index. The value of c was 6.76, and a symptom may appear when K reaches a threshold value Kc = 2.31 X 10(8) (Arieli et al. J Appl Physiol 2002; 92:248-56). METHODS AND RESULTS: The calculation of K for a complex exposure profile made it possible to estimate risk from the normal distribution for a metabolic rate of 1.28 L x min(-1), Z = [ln(K0.5)-9.63]/2.02 and for 0.9 L x min(-1), Z = [ln(K0.5)-11.19]/1.35. The predicted risk was in agreement with the reported risk in composite exposures. The parameters c and ln(Kc) in the power equation are linearly related to metabolic rate (M) and inspired CO2 in rats. Due to the assumed similar relationship between the data from rats and humans, the mean time to CNS oxygen toxicity (tc(M)) as a function of metabolic rate may be calculated for humans as follows: tc(M) = [(e(-2.85 M + 31.8))/(PO2/101.3)(-7.45 M + 39.6)]0.5, where M is metabolic rate in units of resting metabolic rate. A parallel equation for the mean time to toxicity as a function of PCO2 was derived for the rat. This equation can be transformed to express the latency in humans, once the parameters for humans are known. CONCLUSIONS: The power equation that predicts oxygen toxicity in humans was extended to include a complex diving profile as well as the effects of metabolic rate and CO2.

Animals↗

PubMed2003

Hyperoxia may reduce energetic efficiency in the trained rat.

BACKGROUND: Several studies have been conducted in recent years in the attempt to improve running performance by the use of hyperbaric oxygen, but there is disagreement as to whether this has any beneficial effect. The purpose of this study was to measure the effect of 24 h breathing 100% O2 in normobaric conditions on energetic efficiency in the trained rat. METHODS: Experiments were carried out on trained rats whose oxygen consumption was evaluated during the training period and on its completion. At the end of the training period, the rats were divided into two groups: 1) rats exposed to air (21% O2) in normobaric conditions; and 2) rats exposed to 100% O2 in normobaric conditions. In addition, two groups of sedentary rats were used: 3) sedentary rats exposed to air (21% O2) in normobaric conditions; and 4) sedentary rats exposed to 100% O2 in normobaric conditions. Energetic efficiency was estimated by measuring O2 consumption at submaximal exercise (45 m.min-1, 10 degrees incline). RESULTS: Training alone reduced O2 consumption by 18% during submaximal exercise. Exposure to 100% oxygen for 24 h in normobaric conditions reversed the effect of complete training by elevating the O2 consumption by 17%, which was close to the oxygen consumption of the rats during the incomplete training period. CONCLUSIONS: Our results suggest that prolonged exposure to hyperoxia induces a reduction in the energetic efficiency of the trained rat. The relevance of these findings to sports and diving is discussed.

Animals↗

PubMed2002

High-frequency sound field and bubble formation in a rat decompression model.

High-frequency sound might cause bubble enlargement by rectified diffusion. The purpose of the present study was to investigate gas bubble formation in the immersed diving animal during exposure to high-frequency sound. Anaesthetised rats were subjected to a simulated diving profile while immersed inside a hyperbaric chamber. An acoustic beacon (pinger) was placed ventral to the animal's abdomen, transmitting at an intensity of 208.9 dB re 1 micro Pa and a frequency of 37 kHz. Six groups of eight animals were included in the study as in Table 1, breathing air (n = 4) or Nitrox 72/28 (n = 2), at a depth of 0 m, 30 m or 40 m. Immediately after decompression, the intestinal mesenterium was imaged, and frames were acquired digitally. The number of bubbles and their radii were analysed and compared among the groups. The mean bubble density for group 1 was 1.35 +/- 0.18 bubbles/mm(2), significantly higher when compared with the other groups (p < 0.0001). The average bubble radius for groups 1 and 2 was similar (12.57 +/- 4.1 and 10.63 +/- 1.8 microm, respectively), but significantly larger than in the other groups (p < 0.0002). The percentage of bubbles with a radius greater than 50 microm was significantly higher in group 1 (p < 0.0001). The results suggest that commercially available underwater pingers might enhance bubble growth during deep air diving.

Acoustics↗

PubMed2002

Hyperbaric oxygen may reduce gas bubbles in decompressed prawns by eliminating gas nuclei.

It is accepted that gas bubbles grow from preexisting gas nuclei in tissue. The possibility of eliminating gas nuclei may be of benefit in preventing decompression sickness. In the present study, we examined the hypothesis that hyperbaric oxygen may replace the resident gas in the nuclei with oxygen and, because of its metabolic role, eliminate the nuclei themselves. After pretreatment with oxygen, prawns were 98% saturated with nitrogen before explosive decompression at 30 m/min. Ten transparent prawns were exposed to four experimental profiles in a crossover design: 1) 10-min compression to 203 kPa with air; 2) 10-min compression with oxygen; 3) 10-min compression with oxygen to 203 kPa followed by 12 min air at 203 kPa; and 4) 10 min in normobaric oxygen followed by compression to 203 kPa with air. Bubbles were measured after explosive decompression. We found that pretreatment with hyperbaric oxygen (profile C) significantly reduces the number of bubbles and bubble volume. We suggest that hyperbaric oxygen eliminates bubble nuclei in the prawn.

Animals↗