Biomedical subjects

R Arieli

Publications and source records attributed to R Arieli.

At least 19 recordsLinked to original sources

PubMed2025

Oxygen toxicity as a function of time and PO2.

The quantification of O2 toxicity as a function of exposure time (t) and PO2 has been based mainly on the empirical rectangular hyperbola. The non-linear response of the O2-damaged physiological variable (DMG) as a function of time at constant PO2 can be related to the dependence of dDMG/dt on the DMG. The kinetics of the O2-derived chemical species suggests a power relationship between the DMG and PO2 rather than a linear relationship. The combination of time and PO2 considerations suggests two models: 1) DMG = a(ebt - 1) PO2c and 2) DMG = a.tbPO2c, where a, b and c are constant. Non-linear regression of the different parameters of O2 toxicity showed a preference for model 2, with b = 2. Possible mechanisms underlying the kinetics of O2 toxicity and the use of the equation for its prediction are discussed.

Animals↗

PubMed2006

Decompression sickness in the rat following a dive on trimix: recompression therapy with oxygen vs. heliox and oxygen.

Trimix (a mixture of helium, nitrogen, and oxygen) has been used in deep diving to reduce the risk of high-pressure nervous syndrome during compression and the time required for decompression at the end of the dive. There is no specific recompression treatment for decompression sickness (DCS) resulting from trimix diving. Our purpose was to validate a rat model of DCS on decompression from a trimix dive and to compare recompression treatment with oxygen and heliox (helium-oxygen). Rats were exposed to trimix in a hyperbaric chamber and tested for DCS while walking in a rotating wheel. We first established the experimental model, and then studied the effect of hyperbaric treatment on DCS: either hyperbaric oxygen (HBO) (1 h, 280 kPa oxygen) or heliox-HBO (0.5 h, 405 kPa heliox 50%-50% followed by 0.5 h, 280 kPa oxygen). Exposure to trimix was conducted at 1,110 kPa for 30 min, with a decompression rate of 100 kPa/min. Death and most DCS symptoms occurred during the 30-min period of walking. In contrast to humans, no permanent disability was found in the rats. Rats with a body mass of 100-150 g suffered no DCS. The risk of DCS in rats weighing 200-350 g increased linearly with body mass. Twenty-four hours after decompression, death rate was 40% in the control animals and zero in those treated immediately with HBO. When treatment was delayed by 5 min, death rate was 25 and 20% with HBO and heliox, respectively.

Animals↗

PubMed2006

CNS oxygen toxicity in closed-circuit diving: signs and symptoms before loss of consciousness.

INTRODUCTION: There is a dearth of information regarding CNS oxygen toxicity accidents in closed-circuit oxygen diving. The aims of the present study were to report the sensations and symptoms that accompany CNS oxygen toxicity accidents, and to evaluate whether loss of consciousness can occur without any warning signs. METHODS: We documented 36 CNS oxygen toxicity accidents in closed-circuit oxygen diving. The full accident inquiry included the first report from the diving unit, an interview of the victim and his buddy by the researchers, and an examination of the diving equipment. RESULTS: The symptoms that appeared before termination of a dive, as reported by the victim or his buddy, were as follows (in descending order of frequency): limb convulsions; hyperventilation; difficulty maintaining a steady depth; headache; and visual disturbances. The symptoms that appeared after detachment from the mouthpiece were, in descending order of frequency: headache; loss of consciousness; confusion; weakness; dizziness; and facial muscle twitching and limb convulsions. A high inspired CO2 [mean 4.2 kPa (29.9 mmHg)] was connected with loss of consciousness. No dive was terminated before at least two symptoms (mean 3.4) had been noted a minimum of 5 min before termination. DISCUSSION: Symptoms that are accepted as being related to CNS oxygen toxicity, as well as others such as headache, difficulty maintaining a steady depth, hyperventilation, weakness, and a choking sensation, were more frequent among the O2 accident victims compared with divers who did not interrupt their dives. CONCLUSION: Awareness of any unusual sensation can prevent a potentially dangerous situation from arising.

Accidents↗

PubMed2004

Optimal oxygen pressure and time for reduced bubble formation in the N2-saturated decompressed prawn.

Bubbles that grow during decompression are believed to originate from preexisting gas micronuclei. We showed that pretreatment of prawns with 203 kPa oxygen before nitrogen loading reduced the number of bubbles that evolved on decompression, presumably owing to the alteration or elimination of gas micronuclei (Arieli Y, Arieli R, and Marx A. J Appl Physiol 92: 2596-2599, 2002). The present study examines the optimal pretreatment for this assumed crushing of gas micronuclei. Transparent prawns were subjected to various exposure times (0, 5, 10, 15, and 20 min) at an oxygen pressure of 203 kPa and to 5 min at different oxygen pressures (PO2 values of 101, 151, 203, 405, 608, and 810 kPa), before nitrogen loading at 203 kPa followed by explosive decompression. After the decompression, bubble density and total gas volume were measured with a light microscope equipped with a video camera. Five minutes at a PO2 of 405 kPa yielded maximal reduction of bubble density and total gas volume by 52 and 71%, respectively. It has been reported that 2-3 h of hyperbaric oxygen at bottom pressure was required to protect saturation divers decompressed on oxygen against decompression sickness. If there is a shorter pretreatment that is applicable to humans, this will be of great advantage in diving and escape from submarines.

Animals↗

PubMed2004

Effects of nitrogen and helium on CNS oxygen toxicity in the rat.

The contribution of inert gases to the risk of central nervous system (CNS) oxygen toxicity is a matter of controversy. Therefore, diving regulations apply strict rules regarding permissible oxygen pressures (Po(2)). We studied the effects of nitrogen and helium (0, 15, 25, 40, 50, and 60%) and different levels of Po(2) (507, 557, 608, and 658 kPa) on the latency to the first electrical discharge (FED) in the EEG in rats, with repeated measurements in each animal. Latency as a function of the nitrogen pressure was not homogeneous for each rat. The prolongation of latency observed in some rats at certain nitrogen pressures, mostly in the range 100 to 500 kPa, was superimposed on the general trend for a reduction in latency as nitrogen pressure increased. This pattern was an individual trait. In contrast with nitrogen, no prolongation of latency to CNS oxygen toxicity was observed with helium, where an increase in helium pressure caused a reduction in latency. This bimodal response and the variation in the response between rats, together with a possible effect of ambient temperature on metabolic rate, may explain the conflicting findings reported in the literature. The difference between the two inert gases may be related to the difference in the narcotic effect of nitrogen. Proof through further research of a correlation between individual sensitivity to nitrogen narcosis and protection by N(2) against CNS oxygen toxicity in rat may lead to a personal O(2) limit in mixed-gas diving based on the diver sensitivity to N(2) narcosis.

Administration, Inhalation↗

PubMed2002

Modeling pulmonary and CNS O(2) toxicity and estimation of parameters for humans.

The power expression for cumulative oxygen toxicity and the exponential recovery were successfully applied to various features of oxygen toxicity. From the basic equation, we derived expressions for a protocol in which PO(2) changes with time. The parameters of the power equation were solved by using nonlinear regression for the reduction in vital capacity (DeltaVC) in humans: %DeltaVC = 0.0082 x t(2)(PO(2)/101.3)(4.57), where t is the time in hours and PO(2) is expressed in kPa. The recovery of lung volume is DeltaVC(t) = DeltaVC(e) x e(-(-0.42 + 0.00379PO(2))t), where DeltaVC(t) is the value at time t of the recovery, DeltaVC(e) is the value at the end of the hyperoxic exposure, and PO(2) is the prerecovery oxygen pressure. Data from different experiments on central nervous system (CNS) oxygen toxicity in humans in the hyperbaric chamber (n = 661) were analyzed along with data from actual closed-circuit oxygen diving (n = 2,039) by using a maximum likelihood method. The parameters of the model were solved for the combined data, yielding the power equation for active diving: K = t(2) (PO(2)/101.3)(6.8), where t is in minutes. It is suggested that the risk of CNS oxygen toxicity in diving can be derived from the calculated parameter of the normal distribution: Z = [ln(t) - 9.63 +3.38 x ln(PO(2)/101.3)]/2.02. The recovery time constant for CNS oxygen toxicity was calculated from the value obtained for the rat, taking into account the effect of body mass, and yielded the recovery equation: K(t) = K(e) x e(-0.079t), where K(t) and K(e) are the values of K at time t of the recovery process and at the end of the hyperbaric oxygen exposure, respectively, and t is in minutes.

Algorithms↗

PubMed2001

Humidity does not affect central nervous system oxygen toxicity.

Central nervous system (CNS) oxygen toxicity can occur as convulsions and loss of consciousness when hyperbaric oxygen is breathed in diving and hyperbaric medical therapy. Lin and Jamieson (J Appl Physiol 75: 1980-1983, 1993) reported that humidity in the inspired gas enhances CNS oxygen toxicity. Because alveolar gas is fully saturated with water vapor, we could not see a cause and effect and surmised that other factors, such as metabolic rate, might be involved. Rats were exposed to 507- and 608-kPa O(2) in dry (31 or 14%) or humid (99%) atmosphere until the appearance of the first electrical discharge preceding the clinical convulsions. Each rat served as its own control. A thermoneutral temperature (28 +/- 0.4 degrees C) yielded resting CO(2) production of 0.81 +/- 0.06 ml x g(-1) x h(-1). Latency to the first electrical discharge was not affected by humidity. At 507-kPa O(2), latency was 23 +/- 0.4 and 22 +/- 0.7 min in dry and humid conditions, respectively, and, at 608-kPa O(2), latency was 15 +/- 4 and 14 +/- 3 min in dry and humid conditions, respectively. When no effects of CO(2) and metabolic rate are present, humidity does not affect CNS oxygen toxicity. Relevance of the findings to diving and hyperbaric therapy is discussed.

Animals↗

PubMed2001

PCO(2) threshold for CNS oxygen toxicity in rats in the low range of hyperbaric PO(2).

Central nervous system (CNS) oxygen toxicity, as manifested by the first electrical discharge (FED) in the electroencephalogram, can occur as convulsions and loss of consciousness. CO(2) potentiates this risk by vasodilation and pH reduction. We suggest that CO(2) can produce CNS oxygen toxicity at a PO(2) that does not on its own ultimately cause FED. We searched for the CO(2) threshold that will result in the appearance of FED at a PO(2) between 507 and 253 kPa. Rats were exposed to a PO(2) and an inspired PCO(2) in 1-kPa steps to define the threshold for FED. The results confirmed our assumption that each rat has its own PCO(2) threshold, any PCO(2) above which will cause FED but below which no FED will occur. As PO(2) decreased from 507 to 456, 405, and 355 kPa, the percentage of rats that exhibited FED without the addition of CO(2) (F(0)) dropped from 91 to 62, to 8 and 0%, respectively. The percentage of rats (F) having FED as a function of PCO(2) was sigmoid in shape and displaced toward high PCO(2) with the reduction in PO(2). The following formula is suggested to express risk as a function of PCO(2) and PO(2) [abstract: see text] where P(50) is the PCO(2)for the half response and N is power. A small increase in PCO(2) at a PO(2) that does not cause CNS oxygen toxicity may shift an entire population into the risk zone. Closed-circuit divers who are CO(2)retainers or divers who have elevated inspired CO(2)are at increased risk of CNS oxygen toxicity.

Algorithms↗

PubMed2001

Use of a mass spectrometer for direct respiratory gas sampling from the hyperbaric chamber.

BACKGROUND: When conducting respiratory gas measurements during hyperbaric chamber research, it is preferable to carry out gas concentration analysis by mass spectrometry. Gas samples for the mass spectrometer are normally taken from a bypass flow exiting the high pressure chamber to the ambient atmosphere. Under these conditions, mixing in the sampling line smoothes the concentration profile, and much of the advantage of low sampling flow is lost. We propose to use a direct sampling method by mass spectrometer that overcomes these deficiencies. METHODS: In the present study, the original high resistance capillary of a QP 9000 mass spectrometer was inserted through the wall of a hyperbaric chamber. Series A: Air and pure nitrogen flowed alternately (1 s each) via the sampling tip of the mass spectrometer. Series B: End expired CO2 from 15 immersed, professional divers exercising at 405 kPa was measured in a screening test for CO2 retention for nitrox diving. RESULTS: There was no difference in the recorded rise time, fall time and plateau reached in the concentration of oxygen at pressures of 101, 202, 303, 405 and 506 kPa. The new sampling method functioned correctly throughout the full-scale experiment, and the recording of end tidal CO2 was more precise than in the conventional method. CONCLUSIONS. Direct sampling of gases from a hyperbaric chamber by the QP 9000 mass spectrometer has many advantages over sampling of the same gases once they are outside the chamber.

Adult↗

PubMed2000

[Israel Naval Medical Institute: 20 years of applied research, and future goals].

The Israel Naval Medical Institute (INMI) is unique as a research center located in a naval base and having close inter-relations with naval underwater units. It is ideal for applied research, and for mutual exchange of needs and of ideas and instructions. Factors making this institute so suitable for applied research include: direct personal communication with combat divers, professional naval divers, submariners, civilian recreational divers and professional civilian divers, as well as naval vessel crews prone to seasickness; hyperbaric oxygen therapy is administered in cooperation with a large neighboring hospital. Close spatial and personal relations with an academic institution (the Technion, with its Faculties of Medicine, Biology and Biophysics) provide a basis for cooperative research which expands research capabilities, and allows access to extensive expertise, instrumentation and equipment. Close ties with physicians who served at the INMI in the past also bring them into this research community. During their specialization, physicians may spend up to 6 months working with us on a research project. Undergraduate, graduate and post-graduate students may complete their research at our institute with the agreement of their parent academic institutions. Much of the research can be released to the international community. However, some is classified, serves only internal needs or is not of public interest. The number of published papers has stabilized since 1991 at about 16 a year. Studies of gas exchange and oxygen toxicity originate mainly in the Hyperbaric Research Unit, research on motion sickness in the Motion Sickness and Human Performance Laboratory, and work on hyperbaric and diving medicine in the Clinical Section of the INMI.

Academies and Institutes↗

PubMed2000

Can high-frequency sound affect gas-bubble dynamics? A study in the intact prawn Palaemon elegans.

Underwater sound beacons (pingers) are employed in professional and scientific diving for location and navigation. Previous studies have demonstrated that exposure to acoustic fields may lead to the emergence of bubbles and cavities in tissues by rectified diffusion. However, this issue was studied mainly in vitro in various gels and isolated tissues. In the present study, we used the intact prawn Palaemon elegans, whose transparent shell makes it possible to conduct continuous microscopic observation of gas-bubble dynamics in the intact living prawn, to study the effect of high-frequency sound. In a crossover designed experiment, prawns were exposed to hyperbaric pressure of 203 kPa for 10 min, followed by decompression at 40 m/min (control). This procedure was carried out in the study group during transmission of a 37-kHz, 0.25-W, 10-ms pulse width, 1 pulse/s pulse interval. A significant increase was found in the mean volume of bubbles present for a longer period of time, in a higher percentage of the high-frequency sound-exposed prawns. We suggest that this sound exposure causes more gaseous micronuclei to grow into bubbles, and more of the dissolved gas to shift into the gas phase.

Animals↗

PubMed1999

The effect of low-frequency ultrasound on immersed pig lungs.

Acoustic models suggest that high-intensity, low-frequency ultrasound (US) at 21-31 kHz, could cause damage to divers' lungs. The purpose of the study was to investigate lung tissue changes secondary to water-borne low-frequency US produced by commonly used underwater acoustic beacons (pingers). Explanted pig lungs were immersed and exposed to four different modes of low-frequency US pinger transmission. In each trial, 5 pairs of lungs were exposed to sound and 5 pairs served as controls. One central and one peripheral section were taken from each lung and evaluated microscopically for location and extent of damage. When present, microhaemorrhages were primarily found in a patchy alveolar distribution, as well as in the septal and subpleural regions. Only rare focal microhaemorrhages could be found in the Control Group. The results demonstrate a potential hazard to the immersed lungs of large mammals on exposure to prolonged transmission by commercially available underwater pingers. The relevance of these findings to human exposure should be further evaluated.

Animals↗

PubMed1999

Infrared CO2 analyzer error: an effect of background gas (N2 and O2).

Three infrared CO2 analyzers were tested for the effect of background gases: the Ametek CD-3A (Ametek, Thermox Instruments Division, Pittsburgh, PA), the Dräger Multiwarn P CO2 (Dräger, L ubeck, Germany), and the Servomex 1440 (Servomex, Crowborough, East Sussex, UK). Various CO2 concentrations were prepared with Wösthoff precision pumps (H. Wösthoff, Bochum, Germany). Calibration with a different background gas (O2 or N2) caused a similar but systematic error in the CO2 readings of all three analyzers. When the CO2 analyzers were calibrated with N2 as the background gas, the CO2 reading in an O2-enriched atmosphere was 8% lower than the true value. Conversely, calibration with O2 as the background gas resulted in a 10% overestimation of CO2 levels when N2 was the background gas. This error may be important in a few fields of respiratory physiology.

Calibration↗

PubMed1999

Effect of diazepam on survival of the immature pig in a confined atmosphere.

Diazepam is known to prolong survival in an atmosphere containing 5% oxygen, and to reduce cerebral metabolic rate and cerebral perfusion. It also depresses the arousal response to hypoxia and protects the optic nerve from anoxia. We hypothesised that diazepam might extend survival in a confined atmosphere with a limited amount of oxygen. Pigs consumed the oxygen in a sealed chamber until they reached the terminal state. The experimental pigs (n = 6) were sedated with diazepam 0.3 mg/kg i.v. and were compared with a control group (n = 5). We measured blood pressure, inspired O2 and CO2, minute ventilation, ECG, ambient and body temperatures, and PO2, PCO2, O2 content and pH in arterial and venous blood. In the diazepam-treated pigs, oxygen consumption was reduced in the hypoxic range (PIO2 below 60 torr) compared with the control pigs. Diazepam prevented the elevated hypoxic cardiac output found in the control pigs. There were almost no differences between the diazepam and control groups in the other parameters measured in the course of the exposure and in the terminal state. Terminal PIO2, PaO2, and PvO2 were 36.9 +/- 5.6, 27.9 +/- 8.6, 14.3 +/- 2.0 torr, and 36.9 +/- 5.7, 23.7 +/- 7.3, 15.7 +/- 7.6 torr in the diazepam and control groups, respectively. The survival time was 220 +/- 51 and 255 +/- 50 min in diazepam and control pigs, respectively. In spite of its anticonvulsant effect and the fact that it protects CNS white matter from anoxia, prolongs anoxic survival and eliminates the high oxygen demand in hypoxic arousal, diazepam failed to extend hypoxic survival in a confined atmosphere to a lower PIO2. However, diazepam had no deleterious effect on survival, and may therefore be used to ease stressful hypoxic conditions.

Animals↗

PubMed1999

Effect of the anti-motion-sickness medication cinnarizine on central nervous system oxygen toxicity.

Severe seasickness could pose a serious problem in diving, and anti-seasickness medication should therefore be prescribed for the seasickness-susceptible diver. Cinnarizine may be used as a medication if it does not increase the risk of central nervous system (CNS) oxygen toxicity when diving with closed-circuit oxygen or O2-enriched gas mixtures. Twenty-six male, white Sprague-Dawley rats were exposed to high O2 pressures (507 and 608 kPa) before and after cinnarizine ingestion (3.3 mg.kg-1), until the appearance of the first electrical discharge (FED) in the electroencephalogram (EEG) which precedes the clinical convulsions. Each rat was tested on five exposure protocols (control and cinnarizine at 507 kPa O2, control, cinnarizine, and 15 h starvation as a control for cinnarizine at 608 kPa O2) at intervals of at least 2 days or until the EEG connector became detached (a mean of 3.1 exposures per rat). Latency to the FED increased after cinnarizine ingestion in 16 of the 17 pairs of measurements at 507 kPa O2 (by more than 61%, P < 0.002) and in 17 of the 19 pairs of measurements at 608 kPa O2 (by 36%, P < 0.002). There was no significant effect of 15 h starvation. Cinnarizine can be further considered for use in seasickness-susceptible divers as it does not increase the risk of CNS O2 toxicity.

Animals↗

PubMed1998

Latency of oxygen toxicity of the central nervous system in rats as a function of carbon dioxide production and partial pressure of oxygen.

Oxygen toxicity of the central nervous system (CNS) can occur as convulsions and loss of consciousness, with no warning symptoms. A quantitative study of the effect of metabolic rate on sensitivity to oxygen toxicity was made in the rat. A group of 19 rats were exposed (126 exposures) to 12 combinations of four pressures (456, 507, 608 and 709 kPa) and three ambient temperatures (15, 23 and 29 degrees C) until the appearance of the first electrical discharge (FED) preceding clinical convulsions. Carbon dioxide production (VCO2) was also measured. A thermoneutral zone (mean VCO2 0.87 ml x g(-1) x h(-1)) existed between the temperatures of 24 and 29 degrees C; at temperatures lower than this, the metabolic rate increased by 1.2 to 4 times the resting level. Latency of FED decreased linearly with the increase in VCO2 at all four oxygen pressures. The slopes (absolute value) and intercepts decreased with the increase in oxygen pressure. This linear relationship made possible the derivation of an equation which described latency of the FED as a function of both oxygen pressure and metabolic rate. Various environmental and other physiological factors that have been said to influence sensitivity to CNS oxygen toxicity, enhancing the effect of the partial pressure of oxygen, can be explained by their effect on metabolic rate. It is suggested that in situations where there is a risk of oxygen toxicity of the CNS, that risk would be reduced by a lower metabolic rate.

Animals↗

PubMed1997

Recovery time constant in central nervous system O2 toxicity in the rat.

The development of oxygen toxicity can be delayed by intermittent periods of normoxia. However, there is no accepted procedure for quantifing the recovery during normoxia. A cumulative oxygen toxicity index - K, when K reaches a critical value (Kc) and the toxic effect is manifested, can be calculated using the equation K = t(2)e x PO(2)c where t(e) is hyperoxic exposure time and PO2 is oxygen pressure and c is a power parameter. Recovery during normoxia (reducing K) is calculated by the equation K2 = K1 x e(-rt(r)) where t(r) is recovery time, r being the recovery time constant. A combination of accumulation of oxygen toxicity and its recovery can be used to calculate central nervous system oxygen toxicity. In protocol A (n = 25), r was calculated for rats exposed either continuously to 608 kPa oxygen or to PO2 = 608 kPa followed by a period of normoxia (3.5% O2), with a subsequent return to PO2 = 608 kPa until appearance of the first electrical discharge (FED) in the electroencephalogram which precedes clinical convulsions. In protocol B (n = 22), predicted latency to the FED was compared to measured latency for seven different exposures to hyperbaric oxygen (HBO), followed by a period of normoxia and further HBO exposure. Recovery followed an exponential path, with r = 0.31 (SD 0.12) min(-1). The predicted latency to FED in protocol B correlated with the measured latencies. Calculation of the recovery of the CNS oxygen toxicity agreed with the previously suggested exponential recovery of the hypoxic ventilatory response and was probably a general recovery process. We concluded that recovery can be applied to the design of various hyperoxic exposures.

Animals↗

PubMed1997

Thermal status of wet-suited divers using closed circuit O2 apparatus in sea water of 17-18.5 degrees C.

A wet suit may not provide adequate thermal protection when diving in moderately cold water (17-18 degrees C), and any resultant mild hypothermia may impair performance during prolonged diving. We studied heat exchange during a dive to a depth of 5 m in sea water (17-18.5 degrees C) in divers wearing a full wet suit and using closed-circuit oxygen breathing apparatus. Eight fin swimmers dived for 3.1 h and six underwater scooter (UWS) divers propelled themselves through the water for 3.7 h. The measurements taken throughout the dive were the oxygen pressure in the cylinder and skin and rectal temperatures (Tre). Each subject also completed a cold score questionnaire. The Tre decreased continuously in all subjects. Oxygen consumption in the fin divers (1.40 l.min-1) was higher than that of the UWS divers (1.05 l.min-1). The mean total insulation was 0.087 degree C.m2.W-1 in both groups. Mean body insulation was 37% of the total insulation (suit insulation was 63%). The reduction in Tre over the 1st hour was related to subcutaneous fat thickness. There was a correlation between cold score and Tre at the end of 1 h, but not after that. A full wet suit does not appear to provide adequate thermal protection when diving in moderately cold water.

Altitude↗