Search PubMed⌕ Search

Biomedical subjects

R Arieli

Publications and source records attributed to R Arieli.

At least 55 records · Page 3Linked to original sources
PubMed1988

The effect of gravity on the response of ventilation to abrupt change in FICO2.

Recently, Arieli and Farhi (1987) formulated a model for a previous suggestion made by their group that an increased ventilation as gravity increases is due to reduced perfusion of the respiratory center which causes an elevation of tissue PCO2. Extending the model to the dynamic response, we predict a slower ventilatory response to CO2 breathing as gravity increases. To test this prediction, ventilatory response to 5% CO2 was studied in 11 seated subjects at +1 and +2 Gz in a human centrifuge. Five of these subjects were studied at +3 Gz as well. In addition, ventilatory response to 5% CO2, using breath-by-breath analysis, was measured in three subjects in supine and upright postures. The ventilatory response (mainly through tidal volume) was faster as gravity increased from +1 to +2 and to +3 Gz, and from supine to the upright position. These findings disagree with the model prediction. Therefore, an alternative explanation is suggested based on the response of CO2 sensitive stretch receptors in the lung. Increased gravity causes increased ventilation, reduction of cardiac output and increased VA/Q mismatch; all enlarge the part of the lung with low CO2 where responsiveness of the CO2 sensitive stretch receptors is large.

Adult↗
PubMed1988

Oxygen toxicity is not related to mammalian body size.

1. Small mammals have been used to study the effects of O2 toxicity. The aim of the present study was to investigate whether body size should be considered when applying the results of these studies to man. 2. Oxygen toxicity is enhanced as perfusion and metabolism increase: specific animal tissues of high perfusion are more susceptible to O2 toxicity. Exercise, high metabolic rate, and increased brain blood flow enhance O2 toxicity. 3. Increased specific O2 consumption and perfusion as body mass decreases may enhance O2 toxicity in small mammals. 4. Survival time in normobaric hyperoxia (1 atm O2) and the time to first appearance of convulsions in hyperbaric oxygen (4-5 atm) were collected from the literature and showed no relation to body size. 5. Known difference in antioxidant enzyme activity cannot explain the findings. 6. Independence of tissue PO2 on body size, or equal rates of free radical formation and degradation, are suggested as possible mechanisms. 7. Small mammals can serve as a good model for O2 toxicity in man.

Animals↗
PubMed1988

Hyperoxic exposure affects the ventilatory response to hypoxia in awake rats.

We tested whether hyperbaric O2 (HBO) has an adverse effect on the hypoxic ventilatory drive. Four groups of rats were exposed for 550 min to O2 at 1.67, 1.90, and 2.15 ATA and to air at 1.90 ATA, respectively. Ventilatory parameters (frequency, tidal volume, and minute ventilation) were measured using whole-body plethysmography, before the hyperbaric exposure, immediately after the exposure, and up to 20 days after the exposure. Resting ventilation was not affected after exposure at 1.90 ATA to air or at 1.67 ATA to O2. HBO at 1.90 and 2.15 ATA caused a reduction of frequency and an elevation of tidal volume at different inspired gases: air, 5% CO2 balance O2, 80% O2, and 4.5% O2. However, minute ventilation on the day after the hyperoxic exposure was not different from the control at either air, 5% CO2, or 80% O2 but was markedly attenuated on the first three breaths at 4.5% O2. The hypoxic ventilation decreased to 48 +/- 13 (SD) and 32 + 11% after 1.90 and 2.15 ATA, respectively. The ventilatory parameters recovered in the days after HBO. We conclude that HBO reversibly depresses the hypoxic ventilatory drive, most probably by a direct effect on the carotid O2 chemoreceptors.

Animals↗
PubMed1987

Gravity-induced hyperventilation is caused by a reduced brain perfusion.

The suggestion that hyperventilation caused by increased gravity is mediated by a decrease in brain perfusion has led us to propose a mathematical model based on: (1) the CO2 balance equation for the respiratory center (RC), and (2) the relationship between RC blood flow (QRC), foot-to-head acceleration (Gz) and PRCCO2, namely, QRC = [1 - a(Gz - 1)](b X PRCCO2 + c), where the coefficients a, b and c can be calculated from data in the literature. QRC is significantly affected by + GZ only at high PaCO2. The model can be used to calculate oxygen pressure in the RC; the numbers so obtained are in good agreement with measurements of jugular vein PO2 obtained by others.

Blood Flow Velocity↗
PubMed1987

Ventricular electrophysiological properties: is interspecies variability related to thyroid state?

Whereas action potential (AP) duration, area, and repolarization vary considerably, ventricular AP characteristics such as resting membrane potential, AP amplitude, and maximal upstroke velocity of phase 0 depolarization appear similar in a variety of mammalian species. As it has been shown that modifications of the thyroid state are associated with alterations in ventricular electrophysiological properties, we hypothesized that some variations in transmembrane potentials among mammalian species result in part from differences in the individual thyroid states. To test this hypothesis, we used standard microelectrode techniques to study ventricular APs in the dog, mole-rat, guinea pig, rat, mouse, and shrew, which encompass a wide range of thyroid states. In these species O2 consumption ranges from 0.38 (in the shrew) to 4.05 ml O2 X g-1 X h-1 (in the dog). We found that resting membrane potential and AP amplitude, duration, and area were inversely correlated with O2 consumption. The correlation coefficients between these parameters with O2 consumption were -0.92, -0.78, -0.91, and -0.92, respectively. We further tested the hypothesis in guinea pigs in which we modified the thyroid state in opposite directions by thyroxine administration and by propylthiouracil treatment. In the hypothyroid myocardium, AP duration (cycle length = 2,000 ms) markedly increased (P less than 0.001), whereas in the hyperthyroid myocardium, resting membrane potential and AP amplitude (P less than 0.01) and duration (P less than 0.001) decreased. We conclude that interspecies variations in ventricular electrophysiological properties can be correlated with the thyroid state, which may be an important determinant of these properties.

Action Potentials↗
PubMed1986

Hematocrit and hemoglobin concentration in four chromosomal species and some isolated populations of actively speciating subterranean mole rats in Israel.

Hematocrit (HCT) and hemoglobin (Hb) concentration were measured in four chromosomal species and some peripherally semi-isolated and isolated populations of the mole rat superspecies Spalax ehrenbergi in Israel. HCT was 52.0, 51.4, 50.9, and 47.8%, and Hb was 16.0, 16.6, 16.3, and 14.7 g/100 ml for 2n = 52, 58, 54, and 60, respectively. The species 2n = 60, which lives in arid habitats, had lower HCT and Hb than the other three species. HCT decreased as aridity increased between the species and within the species 2n = 60. Changes in HCT probably reflect clinal changes in both soil permeability to gases and ambient temperature.

Animals↗
PubMed1986

Cardiogenic oscillation and phase III caused by pressure-volume heterogeneity: a model.

The effect of heterogeneity of pressure-volume (PV) behavior of lung units and the effect of the pulsations of the heart on expired N2 following a single breath of O2 were studied mathematically in a model of the lung. The lung was pictured as consisting of three compartments, one of high compliance (HC) and another of low compliance (LC), both affected by cardiac pulsations, and a third, nonoscillatory compartment (NC). Three sigmoid PV curves were assigned to the three compartments, for both acini and airway (generation 10-23), so that total compliance summed up to 200 ml/cmH2O. Bifurcation of NC was at generation 5/6 and that of HC and LC at any chosen generation. A steepness constant, K, was defined to characterize the sharply descending portion of the sigmoid PV curve. For a ratio of the steepness constant for the oscillatory compartments, KHC/KLC = 1, a sloping alveolar plateau was produced. The plateau was concave for KHC/KLC greater than 1 and slightly convex for KHC/KLC less than 1. Cardiogenic oscillations (CO) of the expired N2 were produced by alternate flows from either NC or HC and LC. CO diminished in fast expiration, and a phase shift between the heart pulsation and the CO was seen; both agree with experimental findings.

Heart↗
PubMed1986

Effect of water immersion on cardiopulmonary physiology at high gravity (+Gz).

We compared the cardiopulmonary physiology of eight subjects exposed to 1, 2, and 3 Gz during immersion (35 degrees C) to the heart level with control dry rides. Immersion should almost cancel the effects of gravity on systemic circulation and should leave the lung alone to gravitational influence. During steady-state breathing we measured ventilation, O2 consumption (VO2), CO2 production, end-tidal PCO2 (PACO2), and heart frequency (fH). Using CO2 rebreathing techniques, we measured cardiac output, functional residual capacity, equivalent lung tissue volume, and mixed venous O2 content, and we calculated arterial PCO2 (PaCO2). As Gz increased, ventilation, fH, and VO2 rose markedly, and PACO2 and PaCO2 decreased greatly in dry ride, but during immersion these variables changed very little in the same direction. Functional residual capacity was lower during immersion and decreased in both the dry and immersed states as Gz increased, probably reflecting closure effects. Cardiac output decreased as Gz increased in dry rides and was elevated and unaffected by Gz during immersion. We conclude that most of the changes we observed during acceleration are due to the effect on the systemic circulation, rather than to the effect on the lung itself.

Adult↗
PubMed1985

Do the exposure time and PCO2 affect the terminal PO2 in a confined atmosphere?

The effect of exposure time and the presence of CO2 on gas exchange and the terminal PO2 of rats in a confined atmosphere where PO2 decreased due to the oxygen consumption of the rats was measured. Terminal inspired PO2 was higher (46.4 Torr) in short exposure (0.47 h) than terminal PO2 (35.3 Torr) in longer exposures (0.8-13 h). Terminal PO2 was not changed when CO2 accumulated in the sealed chamber (CO2 group) as compared with the conditions where CO2 was consistently removed (no-CO2 group). Carbon dioxide caused further depression of VO2 with developing hypoxia. Both breathing frequency and heart frequency showed no response to PO2 in short exposure, maximal response in intermediate exposure time and reduced response at the longest exposure time. The rat could regulate different physiological parameters to meet its needs in developing hypoxia down to a critical PO2 below which regulation was impaired. This critical PO2 was found to change as a function of the exposure duration. The possible early adjustment to hypoxia and the common use of critical PO2 for comparison between species are discussed.

Animals↗
PubMed1985

Gas exchange in tidally ventilated and non-steadily perfused lung model.

We studied the effect of cyclic lung perfusion - fast cycle in synchrony with heart beats and slow cycle in synchrony with ventilation - on gas exchange in a lung model. There was almost no effect in the fast cycle. In a homogeneous single-lung unit, arterial PO2 increased, and the (A - a)DO2 decreased (by approximately 0.5 Torr), as the amplitude of the slow cyclic lung perfusion (TIP) increased. The calculated (A - a)DO2 and (a - A)DCO2 were negative. Maximal PaO2 was found when peak lung perfusion was delayed with respect to ventilation by 0.2 of a cycle. In a non-homogeneous nine-unit lung, cyclic lung perfusion caused an increase in PaO2 and a decrease in (A - a)DO2 by 2 Torr as compared to steady perfusion. No apparent negative (A - a)DO2 was found, but apparent negative (a - A)DCO2 was calculated at no pulmonary shunt and also with 5% shunt. The correlation of cyclic lung perfusion to the reduced (A - a)DO2 in dense-gas breathing - where large swings of pleural pressure are expected - and its effect on the diffusion capacity of the lung are discussed. Non-steady perfusion of the lung as caused by ventilatory movements expanded our understanding of gas exchange and shed some light on a few controversial experimental findings, such as the negative (a - A)DCO2, the decreased (A - a)DO2 while breathing dense gas, and the effects of gas density on diffusion capacity of the lung.

Functional Residual Capacity↗
PubMed1985

Ventilation and CO2 response during +Gz acceleration.

During foot-to-head acceleration (+Gz) ventilation increases despite a drop in alveolar PCO2. In order to investigate the underlying mechanisms, we measured ventilation (VE), VO2, VCO2 and PACO2, cardiac output (Q) and mixed venous CO2 concentration (CVCO2) using non-invasive techniques in 5 subjects breathing either air or a gas mixture containing 5% CO2 at +1, +2 and +3 Gz in a human centrifuge. Arterial PCO2 was calculated from Fick's equation, using CVCO2, Q and VCO2. VE increased from 8.7 to 18.0 L/min during air breathing and from 19.6 to 36.9 L/min during CO2 breathing at +1 and +3 Gz, respectively. The corresponding values for PACO2 are 37.9 vs 26.9 Torr and 47.8 vs 46.4 Torr. Q dropped from 5.9 to 4.8 L/min during air breathing and remained the same during CO2 breathing (6.7 vs 6.5 L/min). As the decrease of PaCO2 almost paralleled that of PACO2, the arterio-alveolar CO2 difference increased only slightly. The CO2 response curve shifts gradually to the left with an increase in +Gz, a fact that does not support the hypothesis that foot-to-head acceleration increases CO2 sensitivity.

Acceleration↗
PubMed1984

Adaptive respiratory variation in 4 chromosomal species of mole rats.

Oxygen and carbon dioxide pressures were measured in subcutaneous gas pockets of 4 chromosomal species of the Spalax ehrenbergi complex. Oxygen pressures of 11.8, 13.6, 16.9, and 17.2 torr and CO2 pressures of 84.2, 82.9, 80.1, and 64.1 torr were measured for the chromosomal species 2n = 52, 54, 58, and 60, respectively. The differences between the 4 chromosomal species in their subcutaneous gas tension appear to reflect adaptive respiratory variation associated with geographic variation in climate. It underlies an important respiratory physiological correlate of ecological speciation in the extremely hypoxic and hypercapnic subterranean environment.

Animals↗
PubMed1984

Independence of hypoxic death of inspiratory PCO2 in rats and fossorial mole rats.

Laboratory white rats and fossorial mole rats (Spalax ehrenbergi) were subjected to progressive hypoxia by enclosure in a thermoregulated, confined atmosphere. Variable levels of environmental CO2 were obtained by controlling the duration of CO2 absorbance. Rats had preimplanted electroencephalographic (EEG) and electrocardiographic (EKG) electrodes and a rectal temperature probe. Animals were followed until their last gasp and EEG flattening, at which time the chamber's atmosphere was analyzed. The mole rat demonstrated a significantly lower terminal PIO2 [20.9 +/- 3.5 (SD) vs. 38.0 +/- 8.4 (SD) Torr]; however, in both animals terminal PIO2 was independent of PICO2 over a range of the latter of 0-117 Torr. Rats showed a progressive decline in rectal temperature from a PIO2 of 80 Torr on, amounting finally to 2.3 degrees C. The rats' oxygen consumption was maintained down to a PIO2 of 65 Torr and declined from then on. A group of rats with maximal CO2 accumulation showed a greater decline of rectal temperature and a steeper drop of VO2 with respect to PO2 compared to a group with no CO2 buildup. The main result was unexpected, in view of the theoretical synergism of the adverse effects of hypoxia and hypercapnia, and should reorient current thinking on survival and resuscitation in confined spaces.

Animals↗
PubMed1983

Cardiogenic oscillations in expired gas: origin and mechanism.

I produced cardiogenic oscillations (C.O.) of gas concentration for Ar, N2 and CO2 in the expirate by inspiration from RV of a bolus of Ar-O2 mixture followed by O2 to TLC. In 3 out of 4 subjects, C.O. of Ar changed phase during expiration by a half cycle with respect to C.O. of CO2, as was predicted by a previously suggested model (Arieli, R., A.J. Olszowka and H.D. Van Liew (1981) J. Appl. Physiol. 51: 922-928). The model attributed the production of C.O. to fluctuation of the relative flow from two units which differ from each other in their compliance; and due to an assumed dependence of the resistance on the compliance, the time constant of each lung unit changes as a function of lung volume. By scaling the subject's lung volume to Weibel Model A and by the use of expired volume and ECG, I suggest that the origin of C.O. seen at the mouth is at the terminal bronchioles. I made use of the arrhythmic heart rate of one subject to confirm the aligning of ECG with C.O. and also to show that the volume between the site of C.O. origin and the mouth is a function of lung volume. The differences between C.O. of Ar, N2 and CO2 are attributed to their distribution pattern in the lung.

Adult↗
PubMed1981

Exchanges of oxygen and carbon dioxide alter inert gas pattern in single-breath tests.

Concentration of inert gas in the lung is lowered when CO2 entrance exceeds O2 exit and is raised when O2 exit predominates. In air-breathing subjects who expire to residual volume, this "metabolic gas effect" often causes a rising N2 concentration when in fact there should be a terminal fall because of low N2 in apical regions. In single-breath tests, we compared the dilution of resident N2 with dilution of an inspired gas, Ne, to find the "ideal" inert gas concentration (due only to mixing of resident gas with inspired gas). The displacement from the ideal concentration vs. volume pattern depends on the timing of the breath, because early CO2 entrance gives way later to O2 exit. Sometimes observed patterns are above or below but parallel to the ideal, and sometimes the observed slope of phase III is steeper than ideal for N2 and flatter than ideal for Ne. In addition to phase III distortions, the metabolic gas effect sometimes also distorts phase IV height and the intersection between phases III and IV. The distortions depend strongly on absolute concentration of the indicator gas in the lung, so they are very small when "closing volume" maneuvers are done in the conventional manner. However, distortions can be large and misleading when single-breath maneuvers are done in unconventional ways.

Carbon Dioxide↗
PubMed1981

Postinspiratory mixing in the lung and cardiogenic oscillations.

Subjects inspired a 300-ml bolus of indicator gas cocktail (5% each of SF6, Ar, Ne, and He) form residual volume (RV), then inspired air to functional residual capacity (FRC). There was no evidence that a 10-s breath hold changed the relative concentrations or amounts of indicator gases in phases III and IV of expiration or allowed additional gas to mix into the RV, but the breath hold caused cardiogenic oscillations (CO) in expired gas to decrease in height. The units responsible for cardiogenic troughs and peaks are different from the units responsible for phases III and IV, respectively, in that the oscillation troughs had a lower He/SF6 ratio than the peaks whereas phase III had a higher He/SF6 than phase IV. We explain the CO as due to variation in mechanical properties, leading to variation in response to the pressure wave caused by the heart, in units that are relatively near to each other. We conclude that there is little or no postinspiratory mixing between distant lung units, but the dampening of CO suggests that units that are close to each other can mix if time is allowed.

Adult↗
PubMed1981

Corrections for the response time and delay of mass spectrometers.

Computations based on mass spectrometer (MS) outputs will be incorrect unless the delay for drawing the sample into the instrument and response time of the instrument are accounted for. When we changed concentration abruptly in two different mass spectrometers, the responses were sigmoid shaped not exponential, and time constants derived from the main part of the response curves were 43-60 ms; single-exponent corrections using these values caused the corrected waveform to overshoot. For a better correction, we used a two-exponent correction, C2 = Co + (Y1 + Y2) (d2C0/dt) + Y1Y2 (d2C0/dt2), where C0 is MS output as a function of time t, C2 is corrected concentration, and Y1 and Y2 are time constants. Assumption of a third exponent was of little value. For a successful correction Y1 must be smaller than a measured one-exponent time constant. We used two-thirds of the measured value for Y1 and then calculated Y2 from the once-corrected response. The second-order correction approximates a square output in response to a square input. To deal with delay time in a way that would give good resolution of dynamic changes and also be compatible with our response-time correction, we corrected for the difference between time of the input event and time that the output reaches 20% of full response. We validated our methods by integrations of amounts of gases drawn into and out of a syringe and in human breaths.

Argon↗