Changes in transcutaneous tcPO2 during water immersion and its effects on the human body

Changes in transcutaneous PO2(tcPO2) during water immersions with O2 and N2 bubbling are presented. Three healthy male volunteers underwent water immersions for 30 min. Water temperature was controlled to 36.5 degrees C to minimize any thermal stress. Minute ventilation (Ve), oxygen consumption (VO2), heart rate (HR), respiratory rate (RR), and body temperature (Tb) were continuously monitored throughout exposure. In addition, tcPO2 electrode was mounted on the volar side of the right forearm in the middle part of immersion and tcPO2 and tcPCO2 were then monitored in the water. Blood flow of the right forearm was also measured following tcPO2/tcPCO2 measurements The tcPO2 values during water immersions with O2 bubbling were higher than those with N2 bubbling for given blood flow. Although end-tidal PO2 remained unchanged for any occasion, Ve, VO2, HR, RR during water immersions with O2 bubbling were significantly decreased compared to those with N2 bubbling. Results suggest that cutaneous respiration facilitated by hydration may contribute higher tcPO2 values during water immersions with O2 bubbling and may be somewhat related to systemic changes.     

Pressure-time cell death threshold for albino rat skeletal muscles as related to pressure sore biomechanics

Deep pressure sores (DPS) are associated with inadequate soft tissue perfusion and excessive tissue deformation over critical time durations, as well as with ischemia-reperfusion cycles and deficiency of the lymphatic system. Muscle tissue shows the lowest tolerance to pressure injuries, compared with more superficial tissues. In this communication, we present new histopathology data for muscle tissue of albino (Sprague-Dawley) rats exposed to pressures for 15 or 30 min. These data are superimposed with an extensive literature review of all previous histopathology reported for albino rat skeletal muscles subjected to pressure. The pooled data enabled a new mathematical characterization of the pressure-time threshold for cell death in striated muscle of rats, in the form of a sigmoid pressure-time relation, which extends the previous pressure-time relation to the shorter exposure periods. We found that for pressure exposures shorter than 1 h, the magnitude of pressure is the important factor for causing cell death and the exposure time has little or no effect: even relatively short exposures (15 min - 1 h) to pressures greater than 32 kPa (240 mmHg) cause cell death in rat muscle tissue. For exposures of 2 h or over, again the magnitude of pressure is the important factor for causing cell death: pressures greater than 9 kPa (67 mmHg) applied for over 2 h consistently cause muscle cell death. For the intermediate exposures (between 1 and 2 h), the magnitude of cell-death-causing pressure strongly depends on the time of exposure, i.e., critical pressure levels drop from 32 to 9 kPa. The present sigmoidal pressure-time cell death threshold is useful for design of studies in albino rat models of DPS, and may also be helpful in numerical simulations of DPS development, where there is often a need to extrapolate from tissue pressures to biological damage.     

Latency to CNS oxygen toxicity in rats as a function of PCO2 and PO2

Central nervous system (CNS) oxygen toxicity can occur as convulsions and loss of consciousness, without any premonitory symptoms. We have made a quantitative study of the effect of inspired carbon dioxide on sensitivity to oxygen toxicity in the rat. Rats were exposed to four oxygen pressures (PO(2); 456, 507, 608 and 709 kPa) and an inspired partial pressure of carbon dioxide (PCO(2)) in the range 0-12 kPa until the appearance of the electroencephalograph first electrical discharge (FED) that precedes the clinical convulsions. Exposures were conducted at a thermoneutral temperature of 27 degrees C. Latency to the FED decreased linearly with the increase in PCO(2) at all four PO(2) values studied. This decrease, which is probably related to the cerebral vasodilatory effect of carbon dioxide, reached a minimal value that remained constant on further elevation of PCO(2). The slopes (absolute value) and intercepts of latency to the FED as a function of carbon dioxide decreased with the increase in PO(2). This log-linear relationship made possible the derivation of equations that describe latency to the FED as a function of both PO(2) and PCO(2) in the PCO(2) - dependent range: Latency (min) = e((5.19-0.0040)(P)(O(2)))-e((2.77-0.0034)(P)(O(2))) x PCO(2) (kPa), and in the PCO(2)-independent range: Latency(min) = e((2.44-0. 0009)(P)(O(2))). A PCO(2) as low as 1 kPa significantly reduced the latency to the FED. It is suggested that in closed-circuit oxygen diving, any accumulation of carbon dioxide should be avoided in order to minimize the risk of CNS oxygen toxicity.     

Peripheral chemoreflex responsiveness is increased at elevated levels of carbon dioxide after episodic hypoxia in awake humans.

We hypothesized that the acute ventilatory response to hypoxia is enhanced after exposure to episodic hypoxia in awake humans. Eleven subjects completed a series of rebreathing trials before and after exposure to eight 4-min episodes of hypoxia. During the rebreathing trials, subjects initially hyperventilated to reduce the partial pressure of carbon dioxide (Pet(CO(2))) below 25 Torr. Subjects then breathed from a bag containing normocapnic (42 Torr), low (50 Torr), or high oxygen (140 Torr) gas mixtures. During the trials, Pet(CO(2)) increased while a constant oxygen level was maintained. The point at which ventilation began to rise in a linear fashion as Pet(CO(2)) increased was considered to be the ventilatory recruitment threshold. The ventilatory response below and above the recruitment threshold was determined. Ventilation did not persist above baseline values immediately after exposure to episodic hypoxia; however, Pet(CO(2)) levels were reduced compared with baseline. In contrast, compared with baseline, the ventilatory response to progressive increases in carbon dioxide during rebreathing trials in the presence of low but not high oxygen levels was increased after exposure to episodic hypoxia. This increase occurred when carbon dioxide levels were above but not below the ventilatory recruitment threshold. We conclude that long-term facilitation of ventilation (i.e., increases in ventilation that persist when normoxia is restored after episodic hypoxia) is not expressed in awake humans in the presence of hypocapnia. Nevertheless, despite this lack of expression, the acute ventilatory response to hypoxia in the presence of hypercapnia is increased after exposure to episodic hypoxia.     

Separating the effects of hypobaria and hypoxia on lettuce: growth and gas exchange

The objectives of this research were to determine the influence of hypobaria (reduced atmospheric pressure) and reduced partial pressure of oxygen (pO2) [hypoxia] on carbon dioxide (CO2) assimilation (C(A)), dark-period respiration (DPR) and growth of lettuce (Lactuca sativa L. cv. Buttercrunch). Lettuce plants were grown under variable total gas pressures [25 and 101 kPa (ambient)] at 6, 12 or 21 kPa pO2)(approximately the partial pressure in air at normal pressure). Growth of lettuce was comparable between ambient and low total pressure but lower at 6 kPa pO2 (hypoxic) than at 12 or 21 kPa pO2. The specific leaf area of 6 kPa pO2 plants was lower, indicating thicker leaves associated with hypoxia. Roots were most sensitive to hypoxia, with a 50-70% growth reduction. Leaf chlorophyll levels were greater at low than at ambient pressure. Hypobaria and hypoxia did not affect plant water relations. While hypobaria did not adversely affect plant growth or C(A), hypoxia did. There was comparable C(A) and a lower DPR in low than in ambient total pressure plants under non-limiting CO2 levels (100 Pa pCO2, nearly three-fold that in normal air). The C(A)/DPR ratio was higher at low than at ambient total pressure, particularly at 6 kPa pO2- indicating a greater efficiency of C(A)/DPR in low-pressure plants. There was generally no significant interaction between hypoxia and hypobaria. We conclude that lettuce can be grown under subambient pressure ( congruent with25% of normal earth ambient total pressure) without adverse effects on plant growth or gas exchange. Furthermore, hypobaric plants were more resistant to hypoxic conditions that reduced gas exchange and plant growth.     

Effects of controlled gas environments in solid-substrate fermentations of rice

The gas environment is solid-substrate fermentations of rice significantly affected levels of biomass and enzyme formation by a fungal species screened for high amylase production. Constant oxygen and carbon dioxide partial pressures were maintained at various levels in fermentations by Aspergillus oryzae. Control of the gas phase was maintained by a “static” aeration system admitting oxygen on demand and stripping excess carbon dioxide during fermentation. Constant water vapor pressures were also maintained by means of saturated salt solutions. High Oxygen pressures stimulated amylase productivity significantly. On the other hand, amylase production was severely inhibited at high carbon dioxide pressures. While relatively insensitive to oxygen pressure, maximum biomass productivities were obtained at an intermediate carbon dioxide pressure. High oxygen transfer rates were obtained at elevated oxygen pressures, suggesting, in view of the stimulatory effect of oxygen on amylase production, a stringent oxygen requirement for enzyme synthesis. Solid-substrate fermentations were highly advantageous as compared with submerged cultures in similar gas environments. Not only were amylase productivities significantly higher, but the enzyme was highly concentration in the aqueous phase of the semisolid substrate particles and could be extracted in a small volume of liquid. Results of this work suggest that biomass and product formation in microbial processes may be amenable to control by the gas environment. This is believed to offer an interesting potential for optimizing selected industrial fermentation processes with respect to productivity and energy consumption.     

Evidence for an inverse relationship between the ventilatory response to exercise and the maximum whole body oxygen consumption value

Ventilatory responses to submaximal exercise loads indicate that in a population of 895 physically active and sedentary male and female subjects, exercise ventilation is inversely related to predicted VO2max. The correlation coefficients for males and females in this relationship are 0.61 (P less than 0.0001) and 0.26 (P less than 0.0001) respectively. The slopes of regression lines for VE/VO2 and VO2max in female and male subjects are -2.59 and -0.91 respectively. This is associated with changes in composition of the expired air in that PCO2 increases and PO2 decreases with greater VO2max. The difference between the mean oxygen and carbon dioxide partial pressures in expired air of individuals in the highest and lowest VO2max ranges are 1.2 kPa (9 mm Hg) and 0.8 kPa (6 mm Hg) respectively.     

Oxygen uptake during swimming in a hypobaric hypoxic environment

The purpose of this study was to determine oxygen uptake (VO2) at various water flow rates and maximal oxygen uptake (VO2max) during swimming in a hypobaric hypoxic environment. Seven trained swimmers swam in normal [N; 751 mmHg (100.1 kPa)] and hypobaric hypoxic [H; 601 mmHg (80.27 kPa)] environments in a chamber where atmospheric pressure could be regulated. Water flow rate started at 0.80 m.s-1 and was increased by 0.05 m.s-1 every 2 min up to 1.00 m.s-1 and then by 0.05 m.s-1 every minute until exhaustion. At submaximal water flow rates, carbon dioxide production (VCO2), pulmonary ventilation (VE) and tidal volume (VT) were significantly greater in H than in N. There were no significant differences in the response of submaximal VO2, heart rate (fc) or respiratory frequency (fR) between N and H. Maximal VE, fR, VT, fc, blood lactate concentration and water flow rate were not significantly different between N and H. However, VO2max under H [3.65 (SD 0.11) l.min-1] was significantly lower by 12.0% (SD 3.4)% than that in N [4.15 (SD 0.18) l.min-1]. This decrease agrees well with previous investigations that have studied centrally limited exercise, such as running and cycling, under similar levels of hypoxia.     

The critical steady-state hypoxic conditions in carbon tetrachloride-induced lipid peroxidation in rat liver microsomes

Defined steady-state oxygen partial pressures (PO2) were maintained constant with an oxystat system to study carbon tetrachloride (CCl4)-induced lipid peroxidation and oxygen uptake in rat liver microsomes. The initial rates of oxygen uptake and malondialdehyde formation indicated drastically increasing lipid peroxidation by decreasing PO2, attaining a maximum between 1-10 mmHg (0.1-1.3 kPa). Under these conditions, at the hypoxic end of the physiological PO2 in liver, CCl4 caused a 5-fold increase in the oxygen uptake rate and a 20-fold increase in the malondialdehyde formation rate while, at 80 mmHg (10.7 kPa) the haloalkane caused only an increase of 2- and 4-fold, respectively; in comparison, there was only a slight increase in NADPH-induced lipid peroxidation with increasing PO2. These data clearly demonstrate the critical role of low steady-state PO2 in CCl4-induced lipid peroxidation and support lipid peroxidation as a key factor in CCl4 hepatotoxicity.     

Exercise-induced hypoxemia in athletes: Role of inadequate hyperventilation

These experiments examined the exercise-induced changes in pulmonary gas exchange in elite endurance athletes and tested the hypothesis that an inadequate hyperventilatory response might explain the large intersubject variability in arterial partial pressure of oxygen (PaO2) during heavy exercise in this population. Twelve highly trained endurance cyclists [maximum oxygen consumption (VO2max) range = 65-77 ml.kg-1.min-1] performed a normoxic graded exercise test on a cycle ergometer to VO2max at sea level. During incremental exercise at VO2max, 5 of the 12 subjects had ideal alveolar to arterial PO2 gradients (PA-aO2) of above 5 kPa (range 5-5.7) and a decline from resting PaO2 (delta PaO2) 2.4 kPa or above (range 2.4-2.7). In contrast, 4 subjects had a maximal exercise PA-aO2 of 4.0-4.3 kPa with delta PaO2 of 0.4-1.3 kPa while the remaining 3 subjects had PA-aO2 of 4.3-5 kPa with delta PaO2 between 1.7 and 2.0 kPa. The correlation between PAO2 and PaO2 at VO2max was 0.17. Further, the correlation between the ratio of ventilation to oxygen consumption vs PaO2 and arterial partial pressure of carbon dioxide vs PaO2 at VO2max was 0.17 and 0.34, respectively. These experiments demonstrate that heavy exercise results in significantly compromised pulmonary gas exchange in approximately 40% of the elite endurance athletes studied. These data do not support the hypothesis that the principal mechanism to explain this gas exchange failure is an inadequate hyperventilatory response.     

Oxidative stress response of <Emphasis Type="Italic">Kluyveromyces marxianus</Emphasis> to hydrogen peroxide,paraquat and pressure

The aim of this work was to study the oxidative stress response of Kluyveromyces marxianus to hydrogen peroxide (50 mM), paraquat (1 mM), an increase in air pressure (120 kPa, 600 kPa) and pure oxygen pressure (120-600 kPa) in a pressurized bioreactor. The effect of these oxidants on metabolism and on the induction of antioxidant enzymes was investigated. The exposure for 1 h of K. marxianus at exponential growth phase with either H(2)O(2) or paraquat, under air pressure of 120 kPa or 600 kPa, induced an increase in both superoxide dismutase (SOD) and glutathione reductase (GR) content. SOD induction by the chemical oxidants was independent of the air pressure values used. A 2-fold increase in SOD activity was observed after 1 h of exposure to H(2)O(2) and a 3-fold increase was obtained by the presence of paraquat, with both air pressures studied. In contrast, GR activity was raised 1.7-fold by the exposure to both chemicals with 120 kPa, but a 2.4-fold GR induction was obtained with 600 kPa. As opposed to Saccharomyces cerevisiae, catalase was not induced and was even lower than the normal basal levels. This antioxidant enzyme seemed to be inhibited under increasing oxygen partial pressure. The cells showed a significant increase in SOD and GR activity levels, 4.7-fold and 4.4-fold, when exposed for 24 h to 120 kPa pure oxygen pressure. This behaviour was even more patent with 400 kPa. However, whenever cells were previously exposed to low air pressures, low enzymatic activity levels were measured after subsequent exposure to pure oxygen pressure.     

RESPIRATORY EFFECTS UPON THE VISUAL THRESHOLD

Measurements are reported of the effects of respiratory stresses upon the absolute threshold of peripheral (rod) vision. Since subjects were kept wholly dark adapted and the photochemical system of the rods therefore stationary, the changes recorded may be assumed to have originated more centrally. To this degree the measurements provide a quantitative index of central nervous imbalance. Breathing room air or 32 to 36 per cent oxygen at about double the normal rate causes the visual threshold to fall to approximately half the normal value within 5 to 10 minutes. This change is due primarily to alkalosis induced by the hyperventilation, and can be abolished or reversed by adding carbon dioxide to the inspired mixtures. Normal or rapid breathing of 2 per cent carbon dioxide causes no change in threshold; with 5 per cent carbon dioxide the threshold is approximately doubled. Breathing 10 per cent oxygen at the normal rate also approximately doubles the threshold. This effect is compensated in part by rapid breathing. When 10 per cent oxygen is breathed at twice the normal rate the threshold usually falls at first, then slowly rises to supernormal levels. Due primarily to variations in their breathing patterns subjects yield characteristically different responses on sudden exposure to low oxygen tensions with breathing uncontrolled. The threshold may either rise or fall; and on release from anoxia it may rise, or fall to normal or subnormal levels. The threshold adjusts to anoxia rapidly; exposures lasting 5 to 6 hours do not produce greater or more persistent changes than those of much shorter duration.     

Oxygen as a driving gas for nebulisers: safe or dangerous?

Changes in blood gas tensions occurring when 100% oxygen or air was used as the driving gas for nebulised salbutamol were studied in 23 patients with severe airways obstruction. The patients fell into three groups: nine had chronic bronchitis and emphysema with carbon dioxide retention, seven had emphysema and chronic bronchitis without carbon dioxide retention, and seven had severe asthma (no carbon dioxide retention). When oxygen was used as the driving gas patients who retained carbon dioxide showed a mean rise of 1.03 kPa (7.7 mm Hg) in their pressure of carbon dioxide (Pco2) after 15 minutes (p less than 0.001) but the Pco2 returned to baseline values within 20 minutes of stopping the nebuliser. The other two groups showed no rise in Pco2 with oxygen. When air was used as the driving gas none of the groups became significantly more hypoxic. Although it is safe to use oxygen as the driving gas for nebulisers in patients with obstructive airways disease with normal Pco2, caution should be exercised in those who already have carbon dioxide retention.     

Testing Refrigeration Trucks for the Emergency Evacuation of Companion Animals

The purpose of this study was to quantify the changes in oxygen (O₂) and carbon dioxide (CO₂) in sealed refrigerator trucks scheduled to be used for transporting companion animals (dogs and cats) during an emergency evacuation. A total of 122 nonhuman animals (total weight = 1,248 kg) housed in individual crates were loaded into a 16-m refrigeration truck. Once they were loaded, the doors were closed and the percentages of O₂ and CO₂ were measured every 5 min by O₂ and CO₂ analyzers, and they were used to quantify the changes in gas pressure in the sealed truck. CO₂ had a much higher-than-predicted increase, and O₂ had a higher-than-predicted decrease. These 2 pressures in combination with the functionality of the respiratory system will limit the animal's ability to load O₂, and over time, they will initiate asphyxia or suffocation. Over time, the partial pressure of oxygen (P_O2) in the sealed truck will decrease, causing hypoxia, and the partial pressure of carbon dioxide (P_CO2) will increase, causing hypercapnia.     

Exercise tolerance and pulmonary gas exchange after deep saturation dives

Pulmonary function and exercise tolerance were measured before and after three saturation dives to a pressure of 3.7 MPa. The atmospheres were heliox with partial pressures of oxygen of 40 kPa during the bottom phase and 50 kPa during the compression and decompression phase. The bottom times were 3, 10, and 13 days. Decompression time was 13 days. Precordial Doppler monitoring was done daily during the decompression, and an estimate of the total bubble load on the pulmonary circulation was calculated as the accumulated sum of bubble scores recorded for each diver. Nine of the 18 divers had chest symptoms with retrosternal discomfort or nonproductive cough after the dive. There were no changes in dynamic lung volumes. Transfer factor for carbon monoxide was significantly reduced from 12.3 +/- 1.2 to 10.9 +/- 1.3 mmol.kPa-1.min-1 (P less than 0.01), and maximum oxygen uptake was reduced from 3.98 +/- 0.36 to 3.42 +/- 0.37 l/min STPD (P less than 0.01) after the dives. Resting heart rate was increased from 64 +/- 6 to 75 +/- 8 min-1 (P less than 0.01). The ventilatory requirements in relation to oxygen uptake and carbon dioxide elimination were significantly increased (P less than 0.01) after the dives. The physiological dead space fraction of tidal volume was significantly higher and showed an increase with larger tidal volumes (P less than 0.05). Anaerobic threshold estimated from gas exchange data decreased from an oxygen uptake of 2.30 +/- 0.25 to 1.95 +/- 0.28 l/min STPD (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Nitrogen fixation and respiration by root nodules ofAlnus rubra Bong.: Effects of temperature and oxygen concentration

Summary Using a root nodule cuvette and a continuous flow gas exchange system, we simultaneously measured the rates of carbon dioxide evolution, oxygen uptake and acetylene reduction by nodules ofAlnus rubra. This system allowed us to measure the respiration rates of single nodules and to determine the effects of oxygen concentration and temperature on the energy cost of nitrogen fixation. Energy cost was virtually unchanged (2.8–3.5 moles of carbon dioxide or oxygen per mole of ethylene) from 16 to 26°C (pO₂=20 kPa) while respiration and nitrogenase activity were highly temperature dependent. At temperatures below 16°C, nitrogenase activity decreased more than did respiration and as a result, energy cost rose sharply. Acetylene reduction ceased below 8°C. Inhibition of nitrogenase activity at low temperatures was rapidly reversed upon return to higher temperatures. At high temperatures (above 30°C) nitrogenase activity declined irreversibly, while respiration and energy cost increased.Energy cost was nearly unchanged at oxygen partial pressures of 5 to 20 kPa (temperature of 20°C). Respiration and nitrogenase activity were strongly correlated with oxygen tension. Below 5 kPa, acetylene reduction and oxygen uptake decreased sharply while production of carbon dioxide increased, indicating fermentation. Fermentation alone was unable to support nitrogenase activity. Acetylene reduction was independent of oxygen concentration from 15 to 30 kPa. Nitrogenase activity decreased and energy cost rose above 30 kPa until nearly complete inactivation of nitrogenase at 70–80 kPa. Activity declined gradually, such that acetylene reduction at a constant oxygen concentration was stable, but showed further inactivation when oxygen concentration was once again increased. Alder nodules appear to consist of a large number of compartments that differ in the degree to which nitrogenase is protected from excess oxygen.Supported by United States Department of Agriculture Grant 78-59-2252-0-1-005-1     

Effect of a pulsating anti-gravity suit on peak exercise performance in individual with spinal cord injuries

The aim of this study was to examine effects of a pulsating pressure anti-gravity suit on the peak values of oxygen uptake (VO2) and power during maximal arm exercise in spinal-cord-injured (SCI) individuals. Five well-trained SCI men (with lesions at levels between T6 and L1) and seven well-trained able-bodied men (ABC) performed two incremental (10 W x min(-1)) arm-cranking tests. During one test the pressure in the anti-G suit pulsated between 4.7 kPa (35 mmHg) and 9.3 kPa (70 mmHg) every 2 s (PPG+), during the other test (PPG-) all the subjects wore the anti-G suit in a deflated state. Tests were performed in a counter-balanced order. Peak VO2 in SCI was 1 ml x kg(-1) x min(-1) lower during PPG+ compared to PPG- (P = 0.05). Peak power and peak heart rate were not significantly different during PPG+ compared to PPG-. These results would suggest that no increase in work capacity can be obtained with a pulsating pressure anti-gravity suit in either SCI or ABC.     

Fed-batch cultivation of Saccharomyces cerevisiae in a hyperbaric bioreactor

Fed-batch is the dominating mode of operation in high-cell-density cultures of Saccharomyces cerevisae in processes such as the production of baker's yeast and recombinant proteins, where the high oxygen demand of these cultures makes its supply an important and difficult task. The aim of this work was to study the use of hyperbaric air for oxygen mass transfer improvement on S. cerevisiae fed-batch cultivation. The effects of increased air pressure up to 1.5 MPa on cell behavior were investigated. The effects of oxygen and carbon dioxide were dissociated from the effects of total pressure by the use of pure oxygen and gas mixtures enriched with CO(2). Fed-batch experiments were performed in a stirred tank reactor with a 600 mL stainless steel vessel. An exponential feeding profile at dilution rates up to 0.1 h(-)(1) was used in order to ensure a subcritical flux of substrate and, consequently, to prevent ethanol formation due to glucose excess. The ethanol production observed at atmospheric pressure was reduced by the bioreactor pressurization up to 1.0 MPa. The maximum biomass yield, 0.5 g g(-)(1) (cell mass produced per mass of glucose consumed) was attained whenever pressure was increased gradually through time. This demonstrates the adaptive behavior of the cells to the hyperbaric conditions. This work proved that hyperbaric air up to 1.0 MPa (0.2 MPa of oxygen partial pressure) could be applied to S. cerevisiae cultivation under low glucose flux. Above that critical oxygen partial pressure value, i.e., for oxygen pressures of 0.32 and 0.5 MPa, a drastic cell growth inhibition and viability loss were observed. The increase of carbon dioxide partial pressure in the gas mixture up to 48 kPa slightly decreased the overall cell mass yield but had negligible effects on cell viability.     

Further Experiments on the Inhibition of Respiration of Peas Induced by Oxygen at High Pressures

Turner and Quartley (1956) concluded that the tricarboxylicacid cycle was a major respiratory pathway in green shelledpeas subjected to high pressures of oxygen. Additional supportfor this view has been obtained by demonstrating the depletionin content of oxaloacetic acid during treatment with oxygenand by the complete reversal of all the functions determinedfollowing a return of the samples to air after treatment forshort periods with oxygen at high pressures. Oxygen at pressures of either 5 or 3.5 atmospheres caused asimilar pattern in the behaviour of the carbon dioxide production,pH, citric and keto-acids, whilst oxygen at a pressure of 2atm. affected mainly the carbon dioxide production. This suggeststhat the respiration process can be inhibited by oxygen at highpressures in at least two different stages.     

Mechanism of soybean nodule adaptation to different oxygen pressures

Abstract. Soybean nodules showed the ability to adapt to oxygen pressures above and below ambient levels and this adaptation involved a decrease in cortical intercellular air-spaces with increasing oxygen pressure. Nodules were grown in oxygen pressures from 4.7 to 75 kPa and the decrease in number and size of cortical intercellular spaces with increasing oxygen pressure was the result of a change in cell structure and the deposition of an electron dense material within intercellular spaces. Exposure to a saturating pressure of acetylene caused a similar inhibition of respiration and nitrogenase activity in nodules developed in oxygen pressures from 4.7 to 47 kPa, suggesting that putative acetylene-induced changes in oxygen diffusion resistance occur by a different mechanism than that involved in long-term adaptation to oxygen. However, in nodules grown at 75 kPa oxygen, the initial specific activities were lower and did not show an acetylene induced decline. The results are discussed in terms of the current theories of regulation of nitrogenase activity by oxygen availability.