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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↗
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↗
PubMed1996

Effect of exposure time on the survival of immature pigs in a confined atmosphere.

Our purpose if to develop a survival strategy for man trapped in a confined space. A previous study showed that in the rat there is a critical exposure time beyond which hypoxic survival improves. To evaluate the general applicability of these findings in the rat and the influence of body size, the effect of exposure time on hypoxic survival was studied in immature pigs (26 kg). The pig consumed the oxygen in a sealed chamber until hypoxic collapse. We measured blood pressure, oxygen consumption, inspired O2 and CO2, minute ventilation, ECG, body temperature, and PO2, PCO2 and pH in arterial and venous blood. Five groups of pigs were confined in different initial volumes of air, producing total exposure times of 0.5, 1.3, 2.3, 4.8 and 6.7 h. There was no significant difference between the experimental groups for any of the parameters measured during the exposure. Unlike the rat, in the pig there was no "adjustment time" beyond which the animal could survive to a lower PIO2. Terminal inspired PO2 increased as a function of exposure time. This was related to either hypoventilation or lung edema. There was a correlation between the level of carbon dioxide in the blood at 60-70 torr inspired oxygen and the terminal PO2. Pigs which failed to clear the carbon dioxide succumbed early to hypoxia. In a confined space it is preferable to maintain normoxic conditions for as long as possible.

Animals↗
PubMed1995

Effect of accumulation of CO2 on the survival of immature pigs in a confined atmosphere. A: Gas exchange.

Our purpose is to develop a survival strategy for man trapped in a confined space. We used immature pigs to assess the applicability of findings in rats for a larger mammal. The pig consumed oxygen in a sealed chamber until hypoxic collapse. We measured blood pressure, oxygen consumption, inspired O2 and CO2, minute ventilation, ECG and body temperatures, in three groups: no accumulation of CO2; CO2 level maintained at 5%, and maximal accumulation of CO2. Hypoxic oxygen consumption and ventilation were affected by the presence of CO2. Despite the pig's body mass being two orders of magnitude greater than that of the rat, its terminal PIO2 (35.9 torr) did not differ from that of the rat (35.3 torr). Accumulation of CO 2 had no significant effect on the terminal PIO2.

Animals↗
PubMed1995

Effect of accumulation of CO2 on the survival of immature pigs in a confined atmosphere. B: Blood gas exchange.

As part of a study for developing survival strategy for humans in a confined space, we used immature pigs to assess the applicability of findings in rats and to evaluate the effect of body size. The cannulated unanesthetized animal was placed in a sealed chamber and depleted the oxygen until hypoxic collapse. Three groups were: no accumulation of CO2, CO2 maintained at 5%, and maximal accumulation of CO2. In hypoxia arterial and venous oxygen tension were higher in the pigs exposed to CO2 than in the no CO2 pigs. Oxygen extraction increased and oxygen transport decreased in hypoxia in the presence of CO2. Similarity in the P50 of the oxygen dissociation curve may explain the similar terminal PIO2 in the pig and the rat. There was a positive correlation between terminal PIO2 and terminal venous pH.

Animals↗
PubMed1995

CO2 retention during hyperbaric exercise while breathing 40/60 nitrox.

We evaluated CO2 retention in 24 Navy construction divers breathing air at 1 atm abs (101.3 kPa) and 40% O2 (40/60) nitrox at 4 atm abs (Po2 of 162.1 kPa) inside a pressure chamber. The divers sat immersed to the sternal notch and exercised against pneumatically loaded pedals at a Vo2 of approximately 1.3 liter/min. The mean end-tidal CO2 tension (PET(CO2)2) at 1 atm abs (45.7 +/- 5.0 SD torr) was significantly higher than that of non-divers and diving trainees (40 +/- 5.0) but did not increase significantly at depth (47.1 +/- 6.3). The ranking of CO2 retention was not maintained at depth. Unpredictable upward and downward shifts of up to 10 torr occurred in some divers. The PET(CO2) of six of the divers at pressure was greater than 50 torr, which based on animal studies markedly increases the risk of central nervous system oxygen toxicity. We translated their values into individual depth limits with 40/60 nitrox: three with 50 < PET(CO2) < 55 torr were forbidden to dive beyond 25 m and three with values > 55 torr were restricted to 20 m. We propose that whenever possible, PET(CO2) during exercise at pressure be measured in potential nitrox users and that the above PO2 limits be enforced on moderate and extreme CO2 retainers, respectively.

Adult↗
PubMed1995

Epinephrine dose-response of the isolated working heart in O2-exposed rats.

BACKGROUND: Heart energy efficiency, which is affected by catecholamines, has previously been shown to decline in rats with prolonged normobaric O2 exposure. HYPOTHESIS: Oxygen exposure affects dose response of the heart to catecholamines. METHODS: Epinephrine dose-response (10(-10) - 5 x 10(-6) mol.L-1) was measured in the isolated working heart excised from control rats breathing air, and rats exposed to normobaric 100% oxygen for either 24 h or 49 h. The variables measured were input (oxygen consumption (VO2) and output power, cardiac contractility (Emax and maximal dP/dT), coronary resistance, heart frequency (fH) and left ventricular pressure. Variable (Y*) dose response to epinephrine concentration (C) was fitted to the equation: Y* = Ymax/(1 + (C/C50)n), Ymax--maximal Y*, C50--C for half Ymax and n--an empirical power. RESULTS: Oxygen exposure of the intact rat had little influence on baseline cardiac variables, but did affect sensitivity to catecholamines. A general effect of the O2 exposure was a left shift of the dose-response curve for example, C50 was reduced by 72, 41 and 43 x 10-8 mol.L-1 for VO2, fH and Emax, respectively, after the 24 h exposure. CONCLUSIONS: There was a pronounced change in the dose-response in hearts from 24 h O2-exposed rats, a change partially reversed in hearts from 49 h O2-exposed rats. The high dose, which had a stimulatory effect on hearts from control rats, failed to stimulate hearts from hyperoxic rats.

Adrenergic alpha-Agonists↗
PubMed1994

Prediction of central nervous system oxygen toxicity in rats.

Cumulative O2 toxicity (K) can be calculated using the expression K = t2 x PO2c, where t is exposure time and the power c is to be determined; the phenomenon is liable to occur when K reaches Kc, the threshold value of K at which a symptom is manifested. Six rats were each exposed six times to 6 ATA O2 at 2-day intervals until the first electrical discharge (FED) was noted in an electroencephalogram. There was no difference in latency to FED in the series of six exposures. Thirteen rats were exposed to O2 until FED was noted in an electroencephalogram. They were exposed to four constant PO2's of 5, 6, 7, and 8 ATA and to two combined profiles of 1) 5 min at 7 ATA followed by 5 ATA and 2) 15 min at 5 ATA followed by 7 ATA. The solution of the equation for each rat was used to predict its latency to FED on the combined profile. The correlation of predicted to measured latency was significant (P < 0.0001), and the slope was not different from 1. Solving for these parameters using the combination of all the data, we obtained Kc = 5.71 x 10(6) and c = 5.39, which correctly predicted the mean latency but failed to predict individual latency. It is preferable to use each rat as its own control. The significance of the correlation supports the validity of the power equation for calculating K.

Animals↗
PubMed1994

Normoxic, hyperoxic, and hypoxic ventilation in rats continuously exposed for 60 h to 1 ATA O2.

Continuous assessment of ventilation during normobaric hyperoxic exposure may help differentiate between the various effects of hyperoxia on ventilation. Ten rats were exposed continuously to hyperoxia for 60 h with intermittent measurement of ventilation in normoxia, a high-oxygen-mixture (FIO2 > 85%) and hypoxia (FIO2 approximately 1.5%). From the measured parameters of inspiratory and expiratory times (TI and TE) and tidal volume (VT), we calculated breathing frequency (f), minute ventilation (VI), inspiratory drive (VT/TI), TI/(TI+TE) and hypoxic ventilatory drive. Normoxic and high-oxygen-mixture VT increased and f decreased mainly due to increased TI, with no effect on normoxic VI. Hypoxic f and VI decreased as a function of exposure time. The fact that the increase in normoxic VT between 13 and 22 h is followed by an increase in TI between 22 and 30 h, excludes the possibility that sensitization of airway C-fiber receptors causes the increase in VT. There was no correlation between HVD and the inspiratory drive. There would appear to be two stages in O2 toxicity of the ventilatory system: in the first stage, the main effect is on the chemoreflex and mechanoreflex systems, whereas beyond 50 h there are other effects on the lung.

Animals↗
PubMed1993

Hypothermia prolongs survival in a confined atmosphere.

Survival in a confined atmosphere where O2 is limited may be extended by hypothermia. Rats were placed in a thermoregulated sealed chamber which contained a limited amount of air. Rats were studied at low ambient temperatures, in which their terminal rectal temperatures (TB) were 33.2-8.3 degrees C. Rats which had a terminal TB of 20 degrees C achieved maximal O2 extraction. Maximal survival time may be expected with an initial thermoneutral temperature followed by hypothermia with a final TB of 20 degrees C. Resuscitation with no obvious signs of injury was possible after half of the rats succumbed.

Animals↗
PubMed1992

Heart energetic efficiency in O2-exposed rats studied in isolated working heart.

Death in normobaric hyperoxia was related in the past to pulmonary insufficiency of the edematous lung. However, high arterial O2 tension on final collapse led to the suggestion that the heart and not the lung is the first organ that fails. We measured aortic flow, coronary flow, left ventricular pressure, affluent and effluent PO2, PCO2, and pH in the working heart excised from control and normobaric O2-exposed rats (51-63 h). The oxygen consumption (VO2) of experimental hearts was not different from control, but mechanical power output (PVAP) (calculated from pressure-volume area) was reduced as a function of O2 exposure time. Myocardial contractility indexes, maximal elastance and maximal time derivative of pressure, increased as a function of O2 exposure time, being below control values after 50 h and above control values after 60 h. The individual slopes for the regression of VO2 vs. PVAP rose as a function of exposure time from values below control after 50 h exposure to values above control after 60 h. Energetic efficiency (PVAP/VO2) decreased as a function of O2 exposure time and points to possible heart failure in the intact animal. After 50 h O2 exposure the heart was energetically more efficient than the control. Possible changes in the heart are discussed.

Air Pressure↗
PubMed1992

Recovery of the hypoxic ventilatory drive of rats from the toxic effect of hyperbaric oxygen.

Hyperbaric oxygen (HBO) exposure reduces the hypoxic ventilatory drive (HVD), probably by damaging the carotid bodies. The recovery of the HVD from HBO exposure was studied. The HVD was calculated from whole body plethysmographic recordings of the ventilatory response to greater than 85% and 2% O2 in N2 mixtures. Five groups of rats were exposed to HBO for 9 h at pressures of 1.9, 2.0, 2.1, 2.2, and 2.4 ATA, respectively. Each rat underwent three control measurements on different days prior to HBO exposures and then at various intervals following the exposure. Postexposure HVD was reduced to 28% of control values in the high PO2s. Ninety percent recovery of pre-exposure HVD was evident by 12-48 h although in some animals exposed to relatively low PO2s (1.9 and 2.0 ATA) HVD stabilized at a level lower than 100%. The recovery of the HVD in percent during the first 4 d following exposure can be expressed as an exponential function of the time from the termination of HBO: HVD = 28 + 72(1 - exp-0.053t) (t in hours). This information may be of importance in cases of repeated exposures to HBO where one tries to avoid cumulative damage to the carotid bodies, and in the care of the poorly oxygenated patient after HBO treatment.

Air Pressure↗
PubMed1991

Hypoxic survival differs between two mole rat species (Spalax ehrenbergi) of humid and arid habitats.

1. Two chromosomal species, 2n = 52 and 2n = 60 of the mole rat superspecies (Spalax ehrenbergi), occupy humid (2n = 52) and arid (2n = 60) habitats in Israel. 2. Gas conductivity of the soil of the 2n = 52 mole rat is lower than that of the 2n = 60 mole rat, and the 2n = 52 mole rat is better adapted to hypoxia. 3. The hypothesis that the 2n = 52 mole rat can survive to a lower pO2 than the 2n = 60 mole rat was tested. 4. Terminal pO2 (Torr) of four females 2n = 52 was lower, 18.0 +/- 2.9 (SD), than the terminal pO2 of five females 2n = 60, 28.2 +/- 5.1 (SD). 5. The hypoxic survival of the 2n = 52 mole rat as compared to that of the 2n = 60 mole rat correlates with other physiological traits: breathing and heart frequencies, blood hemoglobin and tissue gas tensions.

Acclimatization↗
PubMed1990

Can the rat detect hypoxia in inspired air?

Rats reacted in immediate escape response to encounters with severe hypoxia. This led to a test of the hypothesis that mammals which live in closed spaces (burrows) should have a hypoxic alarm mechanism. A possible detection of hypoxia was studied. Rats were trained to thrust their heads into a compartment flushed by a gas mixture of high or low O2 (balance N2), and after a timed interval, to enter the compartment (on high O2) for a reward or to withdraw (on low O2) to avoid a punishment. Exposure times for the gas mixtures were 5, 3 or 1 sec. The initial conditions for high and low O2 mixtures were 30% and 3% for one series, and 21% and 3% for two other series. Successful discrimination between low and high O2 mixtures led to a stepwise reduction of the concentration difference between them. The rat could detect 21% as different from 30%, 13-17% as different from 21%, and 7-15% as different from 3%. From the short time needed for the learned response (1-3 sec), it is suggested that the rat's olfactory system or airway O2 receptors may be involved in the detection of oxygen.

Animals↗
PubMed1989

Expected pressure-volume heterogeneity within the lung.

Using a model of the lung providing for pressure-volume (P-V) heterogeneity, we reproduced straight (allowing for some concavity or convexity) alveolar plateaus in the nitrogen washout curve with a slope identical to an experimentally measured one (1.2% N2/liter). In a two-unit lung, with one unit of high volume (H) at total lung capacity (TLC) and another of low volume (L) at TLC, three variables could be adjusted to produce the desired alveolar plateaus: the ratio of TLCL/TLCH; the ratio of functional residual capacity, FRCL/FRCH; and the ratio of the steepness constants of their sigmoid P-V curve, KL/KH. We searched for all possible combinations of the three variables that yielded the desired alveolar plateau. For any TLCL/TLCH ratio, there were two single-value solutions for the FRCL/FRCH ratio; thus, the family of solutions was represented by two surfaces in three-dimensional space. We extended the study to a smaller alveolar slope (0.6% N2/liter), assuming that the total slope (1.2% N2/liter) was partially caused by diffusion-convection interaction. We also studied a three-compartment lung as indicative of a multicompartmental lung. The results are discussed in relation to experimentally confirmed P-V heterogeneity. Granting our basic assumptions of P-V heterogeneity, the real physical lung characteristics may be a subsection of the range of theoretical solutions described herein.

Adult↗
PubMed1989

Attenuation of hypoxic ventilation by hyperbaric O2: effects of pressure and exposure time.

Hyperoxia affects O2 chemoreception in the highly perfused carotid bodies and causes a reduction of the ventilatory hypoxic drive (HD) as was shown for anesthetized cats and awake rats. We looked for a quantitative description of such an effect on HD as a function of both O2 pressure and exposure duration. Ventilation of rats was measured using the barometric method before and after hyperbaric O2 (HBO) exposure, at either air, 80% O2, or 4% O2. We used three exposure durations: 180, 550 and 900 min. The O2 pressure ranged between 1.2 and 3.0 ATA. At each time duration we used four to five groups of rats at a range of O2 pressures that yielded the full scale of effect on HD but avoided obvious lasting difficulties in breathing. HBO caused a reduction of breathing frequency and elevation of tidal volume in both air and 80% O2 but almost no change in minute ventilation. Hypoxic minute ventilation (4% O2) decreased after HBO, mainly through reduced frequency. HD was described by a power function of O2 pressure for each HBO duration. HD did not decline below 20% of the full control response. Ventilatory HD diminution is pictured as a function of both O2 pressure and HBO duration. The dependency of HD on exposure time and on pressure is similar to other known toxic effects of HBO.

Animals↗