Breathing Gas Mixtures Research Articles

Rapid Design of an ICU Ventilator: An Approach Based on Smart Switching of Compressed Air-Oxygen.

Breathing support is provided by regulating volume or pressure of lungs using ventilators. Due to COVID-19 pandemic, there was a sudden shortage of resuscitating devices such as ventilators. Additionally, ventilators being one of the primary critical care devices are also very costly. In order to address this situation, a number of low-cost designs have been proposed, however, many of these lack either an efficient control system or a hardware comparable to a standard ICU ventilator. In this regard, this article presents a comprehensive cost-effective solution that covers all aspects of the ventilator design (named as NED-Vent) such as hardware/pneumatic assembly, electronic design, user interface and control system. The proposed design works on compressed air-oxygen switching via proportional valves to produce basic volume and pressure modes as well as their derivatives such as assist ventilation, intermittent ventilation and spontaneous modes. The NED-Vent also features an interactive single-knob-single-touch user interface along with an automated mechanism for adjusting air-oxygen ratio in breathing gas mixture as an improvement on existing designs. The pressure regulated control is based on two mathematical models of human lungs with dynamic lung parameters estimated using machine learning approach. Additionally, the controller is tuned to optimized stability using Jury's Test and Ziegler-Nichols methods. The obtained results of breath profile are validated for the employed mathematical models (SLSC & SLMC) as well as the tuning methods in compliance with the tolerances provided by international standards.

Effect of acute heat exposure on the pressor response to a voluntary hypoxic apnea.

The pressor response induced by a voluntary hypoxic apnea is mediated largely by increased sympathetic outflow. The neural control of blood pressure is altered in recovery from acute heat exposure, but its effect on the pressor response to a voluntary hypoxic apnea has never been explored. Therefore, we tested the hypothesis that prior heat exposure would attenuate the pressor response induced by a voluntary hypoxic apnea. Eleven healthy adults (five women) were exposed to whole body passive heating (water-perfused suit) sufficient to increase body core temperature by 1.2°C. Voluntary hypoxic apneas were performed at baseline and in recovery when body core temperature returned to ≤ 0.3°C of baseline. Participants breathed gas mixtures of varying [Formula: see text] (21%, 16%, and 12%; randomized) for 1 min followed by a 15-s end-expiratory apnea. The change in arterial oxygen saturation during each apnea did not differ from baseline to recovery (P = 0.6 for interaction), whereas the pressor response induced by a voluntary hypoxia apnea was reduced ([Formula: see text] 21%, baseline 17 ± 7 mmHg vs. recovery 14 ± 7 mmHg; [Formula: see text] 16%, baseline 24 ± 8 mmHg vs. recovery 18 ± 7 mmHg; [Formula: see text] 12%, baseline 28 ± 11 mmHg vs. recovery 24 ± 11 mmHg; P = 0.01 for main effect of time). These data suggest that prior heat exposure induces a cross-stressor effect such that the pressor response to a voluntary hypoxic apnea is attenuated.NEW & NOTEWORTHY The pressor response induced by a voluntary hypoxic apnea is mediated by increased sympathetic outflow. The neural control of blood pressure is altered in recovery from acute heat exposure, but its effect on the pressor response to a voluntary hypoxic apnea has never been explored. Our data suggest that prior heat exposure induces a cross-stressor effect such that the pressor response to a voluntary hypoxic apnea is attenuated.

Influence of breathing gas mixtures with increased partial pressure of oxygen on the state of the diver’s body functions

Influence of breathing gas mixtures with increased partial pressure of oxygen on the state of the diver’s body functions

Effect of Acute Heat Exposure on the Pressor Response to a Voluntary Hypoxic Apnea: A Cross‐Tolerance Study

The pressor response induced by a voluntary hypoxic apnea is exaggerated in individuals with obstructive sleep apnea and is strongly correlated to sympathetic overactivity. Acute heat exposure alters neural control of blood pressure, but its effect on the pressor response to a voluntary hypoxic apnea has never been explored. Therefore, we tested the hypothesis that acute heat exposure would attenuate the pressor response to a voluntary hypoxic apnea, and thereby manifest as a form of physiological cross‐tolerance. Six young adults (2 females, 25 ± 1 yrs) were exposed to passive heat stress (water‐perfused suit) sufficient to increase body core temperature by 1.2 °C. Voluntary hypoxic apneas were performed in duplicate before acute heat exposure (pre‐heat) and in recovery when body core temperature returned to ≤ 0.3 °C of baseline. Participants breathed gas mixtures of varying FiO2 (21%, 16%, and 12%; randomized) for 1 min followed immediately by a 15 s end‐expiratory apnea. Beat‐by‐beat arterial blood pressure (Finometer) and arterial oxygen saturation (finger pulse oximetry) were measured throughout. The pressor response was calculated as the difference between baseline mean arterial pressure and the peak response following each apnea. The change in arterial oxygen saturation during each apnea did not differ from pre‐heat to recovery (FiO2 21%: pre‐heat, Δ0 ± 1 % vs. recovery, Δ1 ± 2 %; FiO2 16%: pre‐heat, Δ‐4 ± 1 % vs. recovery, Δ‐3 ± 1 %; FiO2 12%: pre‐heat, Δ‐9 ± 3 % vs. recovery, Δ‐10 ± 4 %; P = 0.6 for interaction). The pressor response to a voluntary apnea was attenuated in recovery from acute heat exposure across all gas mixtures (FiO2 21%: pre‐heat, Δ14 ± 11 mmHg vs. recovery, Δ10 ± 7 mmHg; FiO2 16%: pre‐heat, Δ22 ± 15 mmHg vs. recovery, Δ15 ± 11 mmHg; FiO2 12%: pre‐heat, Δ28 ± 15 mmHg vs. recovery, Δ21 ± 16 mmHg; P < 0.01 for main effect of time). These data suggest that acute heat exposure induces a cross‐tolerance effect such that the pressor response to a voluntary hypoxic apnea is reduced. Acute heat exposure could improve hypertension in adults with obstructive sleep apnea, secondary to altered chemoreflex function and sympathetic neural control, and provide additional therapeutic options for this population to improve cardiovascular health.

Role of hyperpnea in the relaxant effect of inspired CO2 on methacholine-induced bronchoconstriction.

Inhaling carbon dioxide (CO2) in humans is known to cause inconsistent effects on airway function. These could be due to direct effects of CO2 on airway smooth muscle or to changes in minute ventilation (V̇e). To address this issue, we examined the responses of the respiratory system to inhaled methacholine in healthy subjects and subjects with mild asthma while breathing air or gas mixtures containing 2% or 4% CO2. Respiratory mechanics were measured by a forced oscillation technique at 5 Hz during tidal breathing. At baseline, respiratory resistance (R5) was significantly higher in subjects with asthma (2.53 ± 0.38 cmH2O·L-1·s) than healthy subjects (2.11 ± 0.42 cmH2O·L-1·s) (P = 0.008) with room air. Similar values were observed with CO2 2% or 4% in the two groups. V̇e, tidal volume (VT), and breathing frequency (BF) significantly increased with CO2-containing mixtures (P < 0.001) with insignificant differences between groups. After methacholine, the increase in R5 and the decrease in respiratory reactance (X5) were significantly attenuated up to about 50% with CO2-containing mixtures instead of room air in both asthmatic (P < 0.001) and controls (P < 0.001). Mediation analysis showed that the attenuation of methacholine-induced changes in respiratory mechanics by CO2 was due to the increase in V̇e (P = 0.006 for R5 and P = 0.014 for X5) independently of the increase in VT or BF, rather than a direct effect of CO2. These findings suggest that the increased stretching of airway smooth muscle by the CO2-induced increase in V̇e is a mechanism through which hypercapnia can attenuate bronchoconstrictor responses in healthy subjects and subjects with mild asthma.NEW & NOTEWORTHY The main results of the present study are as follows: 1) breathing gas mixtures containing 2% or 4% CO2 significantly attenuated bronchoconstrictor responses to methacholine, not differently in healthy subjects and subjects with mild asthma, and 2) the causal inhibitory effect of CO2 was significantly mediated via an indirect effect of the increment of V̇e in response to intrapulmonary hypercapnia.

Physiological effects of mixed-gas deep sea dives using a closed-circuit rebreather: a field pilot study.

Deep diving using mixed gas with closed-circuit rebreathers (CCRs) is increasingly common. However, data regarding the effects of these dives are still scarce. This preliminary field study aimed at evaluating the acute effects of deep (90-120msw) mixed-gas CCR bounce dives on lung function in relation with other physiological parameters. Seven divers performed a total of sixteen open-sea CCR dives breathing gas mixture of helium, nitrogen and oxygen (trimix) within four days at 2 depths (90 and 120msw). Spirometric parameters, SpO2, body mass, hematocrit, short term heart rate variability (HRV) and critical flicker fusion frequency (CFFF) were measured at rest 60min before the dive and 120min after surfacing. The median [1st-3rd quartile] of the forced vital capacity was lower (84% [76-93] vs 91% [74-107] of predicted values; p = 0.029), whereas FEV1/FVC was higher (98% [95-99] vs 95% [89-99]; p = 0.019) after than before the dives. The other spirometry values and SpO2 were unchanged. Body mass decreased from 73.5kg (72.0-89.6) before the dives to 70.0kg (69.2-85.8) after surfacing (p = 0.001), with no change of hematocrit or CFFT. HRV was increased as indicated by the higher SDNN, RMSSD and pNN50 after than before dives. The present observation represents the first original data regarding the effects of deep repeated CCR dives. The body mass loss and decrease of FVC after bounce dives at depth of about 100msw may possibly impose an important physiological stress for the divers.

Exposure to hypoxia impairs helicopter pilots’ awareness of environment

The purpose of the present study was to determine how hypoxia effects awareness of environment (AoE) in helicopter pilots operating at high altitude. Eight helicopter crews flew two operational flights in a flight simulator while breathing gas mixtures of 20.9% (equivalent to 0 m altitude) and 11.4% (equivalent to 4572 m or 15,000 ft altitude) oxygen in a single blinded, counterbalanced, repeated measures study. Each flight included five missions, during which environment items were introduced that the crews needed to be aware of, and respond to. In the 4572 m simulation, the crews missed overall 28 AoE items compared to 12 in the 0 m simulation (Z = −1.992; p = .046). In contrast, the crews’ technical skills were not significantly effected by hypoxia. Remarkably, the majority of pilots did not notice they were hypoxic or recognise their hypoxia symptoms during the simulation flight at 4572 m. Practitioner summary We show that hypoxia has a detrimental effect on helicopter pilot’s AoE and alertness. This can lead to an increased risk for flight safety. To mitigate this risk we recommend performing hypoxia training in a flight simulator, developing wearable systems for physiological monitoring of pilots and re-evaluating current altitude regulations. Abbreviations: ANOVA: Analysis of variance; AoE: awareness of environment; CSV: comma-separated values; HDU: helmet display unit; HR: heart rate; IQR: interquartile range; Mdn: median; NTS: non-technical skills; RNLAF: Royal Netherlands Air Force; PPM: parts per million; SpO2: oxygen saturation; SSS: Stanford sleepiness scale; TS: technical Skills

Relationship between breathing gas mixtures and retinal vessel regulation

PurposeIt is known that components of oxygen transport pathway communicate with vascular endothelium. However, oxygen‐induced vessel constriction results in a decrease in retinal blood flow. Because the delivery and removal of metabolites and gases is proportional to blood flow, a decrease in blood flow could have deleterious effects. Due to the systemic nature of the endothelium, this should be taken into account wherever breathing gas mixture is changed (anesthesia). This work aims to clarify how the constriction of the retinal vessels is modulated by breathing gas mixtures using dynamic vessel analysis (DVA).MethodsThe baseline diameters of 15 volunteers (9 m, 26.3 ± 3.3 y) were measured using DVA (Imedos Systems GmbH). We investigated four primary vessel segments (superior as well as inferior temporal artery (STa/ITa) and vein (STv/ITv). For each volunteer, the DVA was performed 5 times (each: duration 15 min [1 min baseline, 8 min gas mixture, 6 min recovery], rest period: 10 min) in a randomized order using different gas mixtures (21%, 30%, 40%, 50%, 60% O2) provided by a ventilator (Bellavista 1000, imtmedical AG). For statistical analysis, the t‐test and the Wilcoxon test for paired samples (Bonferroni corrected) were used.ResultsFor all vessel segments, a stronger constriction could be observed with an increase in the oxygen concentration. The maximum constriction was always measured at the end of the 8 min period. Here, when comparing the constriction values of the 21% O2 concentration, already the 30% O2 concentration showed significant changes (30%/40%/50%/60% STa: p = 0.002/0.001/0.000/0.000, ITa: p = 0.001/0.001/0.001/0.000, STv: p = 0.000/0.000/0.000/0.000, ITv: p = 0.001/0.000/0.000/0.000).ConclusionsThe presented work revealed that even a small change in breathing gas mixture causes a significant change in vessel constriction. These effect is not only to be expected at the retina, but also in the brain as an example. This should be taken into account, amongst others, for longer anesthesia.

Parvalbumin Expression in Rat Subventricular Zone as Affected by Acute Hypoxia during Early Postnatal Ontogeny

This study aimed to reveal parvalbumin (PVA) expression in cells of the subventricular zone (SVZ), identify the morphological type of these cells, and estimate the effect of acute hypoxia on the size of this cell population in the Wistar rat neonatal period. PVA-expressing cells were revealed immunohistochemically using Abcam rabbit polyclonal antibodies to this calcium-binding protein. Rats were exposed to hypoxia in a special chamber with 7.8% oxygen in a breathing gas mixture. The brain was examined in the neonatal period on postnatal days 5 and 10. It was found that the SVZ, both in control and experimental rats, contains PVA- expressing cells of the same morphological type, which represent migrating immature neuroblasts (type A). In control animals, throughout the entire neonatal period, the number of these cells remains constant and accounts for more than 20% of the total cell population. Perinatal hypoxic exposure leads to increase the number of PVA-expressing cells, as well as the total number of cells, in the SVZ (to 33%). Thus, perinatal hypoxia activates neurogenesis in the SVZ during the neonatal period. In the same period, some neuroblasts express PVA and may reach a certain degree of differentiation of their neurotransmitter phenotype.

ЭКСПРЕССИЯ ПАРВАЛЬБУМИНА В КЛЕТКАХ СУБВЕНТРИКУЛЯРНОЙ ЗОНЫ И ВЛИЯНИЕ НА НИХ ОСТРОЙ ГИПОКСИИ В РАННИЙ ПОСТНАТАЛЬНЫЙ ПЕРИОД У КРЫС

This study aimed to reveal parvalbumin (PVA) expression in cells of the subventricular zone (SVZ), identify the morphological type of these cells, and estimate the effect of acute hypoxia on the size of this cell population in the Wistar rat neonatal period. PVA-expressing cells were revealed immunohistochemically using Abcam rabbit polyclonal antibodies to this calcium-binding protein. Rats were exposed to hypoxia in a special chamber with 7.8% oxygen in a breathing gas mixture. The brain was examined in the neonatal period on postnatal days 5 and 10. It was found that the SVZ, both in control and experimental rats, contains PVA-expressing cells of the same morphological type, which represent migrating immature neuroblasts (type A). In control animals, throughout the entire neonatal period, the number of these cells remains constant, accounting for more than 20% of the total cell population. Perinatal hypoxic exposure leads to increase the number of PVA-expressing cells, as well as the total number of cells, in the SVZ (to 33%). Thus, perinatal hypoxia activates neurogenesis in the SVZ during the neonatal period. In the same period, some neuroblasts express PVA and may reach a certain degree of differentiation of their neurotransmitter phenotype.

Experimental Installation used for Preparation of Breathing Mixtures Needed for Professional Diving

Starting from the mathematical modelling of the gas dynamics processes and, of course, from the needs of the Diving Center, several schemes of experimental installations were developed. These schemes are used for the preparation of binary or ternary gas mixtures, specific: for autonomous professional diving, for the system diving, respectively for those simulated or real which are performed in the hyperbaric chambers of the Diving Center or in the diving turrets.The principle of preparing breathing gas mixtures in the experimental installation ensures that an invariable flow rate (with the pressure of the gaseous mixture from a pressurized cylinder) is injected (constant mass flow) while ensuring the permanent control of this flow. The installation delivers an invariable gas mixture flow regardless of the gas pressure value inside the storage cylinder.Depending on the number of components from which the binary or ternary breathable mixture is to be prepared, the design of the plant has been structured in two parts or in the case of a more complex ternary structure of the gaseous mixture, the plant has three distribution-injection lines active. Each of these lines independently carries the three pure component gases used to continuously produce the required respiratory mixture.Finally, the tests of the gas-dynamical processes related to the plant were presented very succinctly, following a comprehensive testing and evaluation plan in the summer of last year.

Renal Adaptive Changes in Response to Chronic Metabolic or Respiratory Acidosis: Regulation of Expression of Acid‐base Transporters and Enzymes

Kidneys excrete acid loads mainly by generating and excreting total ammonia (NH3plus NH4+) and to a lesser extent titratable acids (TA). Urinary excretion of NH3/NH4+ and TAincreases significantly in acidosis. We made the assumption that this augmented urinary acid excretion (NH3/NH4+and TA) will differ depending on the type of acid‐load. To test this hypothesis, we conducted in‐vivo experiments on mice to measure urinary NH3/NH4+and TA under metabolic or respiratory acid loads and investigated expression of carbonic anhydrase and acid‐base transporters by Western analysis.We induced metabolic acidosis in 2 groups of mice: one group received an acid diet (AD) supplemented with 0.4N HCl (at 1mg/g of chow); a second group received drinking water fortified with NH4Cl (0.28M) and 1% sucrose (NH4+‐W); a control group received normal diet (ND). Our data showed that urinary NH4+(u‐NH4+) increased gradually in mice on AD or NH4–W diet compared to control (ND) and the increase in u‐NH4+was proportionally higher than that of TA. Unexpectedly, expression of the NH3/NH4+transporters, Rhbg and Rhcg, in both groups of acid‐loaded mice was not significantly different compared to mice on ND. An interesting finding, however, was that expression of CA‐IV was reduced in both acidosis groups. In mice on AD, RNAseq data showed that carbonic anhydrase‐II (CA‐II) was upregulated whereas pendrin (a Cl‐HCO3−exchanger) expression was downregulated.We induced chronic respiratory acidosis by placing mice for 3 days in special chambers where breathing gas mixtures were 8% CO2(balance 21% O2&amp; 71% N2). A control group breathed normal air. There were no significant changes in urinary excretion of TA in both hypercapnic or control groups. However, urinary NH4+in hypercapnic mice increased significantly after 24 hours and continued to gradually increase in days 2 and 3. In control mice, there was a small increase in urinary NH4+excretion in day 1 (p &lt; 0.05), probably caused by housing distress in metabolic cages, but leveled off in days 2 and 3. Western analysis showed that hypercapnia induced a marked increase in expression of Rhbg but only a moderate increase of Rhcg. Chronic hypercapnia increased expression of CA‐IV significantly but decreased expression of pendrin.In summary, we demonstrated that renal response to acidosis varies with the type of acid load. High CO2 acidosis downregulated pendrin even though plasma HCO3−is high. In metabolic acidosis, the increase in urinary NH4+is likely caused by increased ammoniagenesis, whereas upregulation of NH3/NH4+transporters is more evident in respiratory than in metabolic acidosis. These data show a link among chronic hypercapnia, NH4+excretion and expression of the NH3/NH4+transporters, Rhbg and Rhcg. These studies are important to understand the renal mechanisms of correcting respiratory and metabolic acidosis.Support or Funding InformationU54 GM104940 from NIH, VA Merit grant, NIH‐RO1, Carol Lavin Bernick grant and Tulane Bridge grantThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Modeling the process of chemical regeneration of air in airtight habitable facilities

Physical experiments and mathematical modeling are used to study the kinetics of the reactions of carbon dioxide and water with potassium superoxide accompanied by oxygen release at various values of the temperature and humidity of the breathing gas mixture. The kinetics of the chemisorption is demonstrated to be limited by the rate of air regeneration in an airtight habitable facility. Experimental and analytical approaches are applied to determine the kinetic coefficients of the chemical reactions using the experimental data and a mathematical model of chemisorption kinetics. To perform the above chemical reactions, an original-design chemisorption reactor was developed, which contains plates with potassium superoxide nanocrystalline fixed on the fibers and pore surface of a fibrous polymer matrix. A mathematical model of chemical air regeneration is developed to calculate the guaranteed values of the parameters of the reactor and the protective effect time of the chemisorbent during which, at a given load, the reactor provides the appropriate concentrations of oxygen and carbon dioxide in the breathing gas mixture in an airtight habitable.

Increased PIO2 at Exhaustion in Hypoxia Enhances Muscle Activation and Swiftly Relieves Fatigue: A Placebo or a PIO2 Dependent Effect?

To determine the level of hypoxia from which muscle activation (MA) is reduced during incremental exercise to exhaustion (IE), and the role played by PIO2 in this process, ten volunteers (21 ± 2 years) performed four IE in severe acute hypoxia (SAH) (PIO2 = 73 mmHg). Upon exhaustion, subjects were asked to continue exercising while the breathing gas mixture was swiftly changed to a placebo (73 mmHg) or to a higher PIO2 (82, 92, 99, and 142 mmHg), and the IE continued until a new exhaustion. At the second exhaustion, the breathing gas was changed to room air (normoxia) and the IE continued until the final exhaustion. MA, as reflected by the vastus medialis (VM) and lateralis (VL) EMG raw and normalized root mean square (RMSraw, and RMSNz, respectively), normalized total activation index (TAINz), and burst duration were 8–20% lower at exhaustion in SAH than in normoxia (P < 0.05). The switch to a placebo or higher PIO2 allowed for the continuation of exercise in all instances. RMSraw, RMSNz, and TAINz were increased by 5–11% when the PIO2 was raised from 73 to 92, or 99 mmHg, and VL and VM averaged RMSraw by 7% when the PIO2 was elevated from 73 to 142 mmHg (P < 0.05). The increase of VM-VL average RMSraw was linearly related to the increase in PIO2, during the transition from SAH to higher PIO2 (R2 = 0.915, P < 0.05). In conclusion, increased PIO2 at exhaustion reduces fatigue and allows for the continuation of exercise in moderate and SAH, regardless of the effects of PIO2 on MA. At task failure, MA is increased during the first 10 s of increased PIO2 when the IE is performed at a PIO2 close to 73 mmHg and the PIO2 is increased to 92 mmHg or higher. Overall, these findings indicate that one of the central mechanisms by which severe hypoxia may cause central fatigue and task failure is by reducing the capacity for reaching the appropriate level of MA to sustain the task. The fact that at exhaustion in severe hypoxia the exercise was continued with the placebo-gas mixture demonstrates that this central mechanism has a cognitive component.

Beneficial Properties of Argon After Experimental Subarachnoid Hemorrhage: Early Treatment Reduces Mortality and Influences Hippocampal Protein Expression.

Until now, treatment ameliorating early brain injury following subarachnoid hemorrhage has been nonexistent. Here, we evaluate the neuroprotective properties of argon after experimental subarachnoid hemorrhage with mortality as the primary endpoint and functional outcome, as well as hippocampal cellular and molecular stress response as secondary endpoints. Randomized controlled animal study. University research laboratory. Ninety-eight male Sprague-Dawley rats. One hour after subarachnoid hemorrhage induction via endovascular perforation technique or sham surgery, a breathing gas mixture containing 50 vol% argon/50 vol% oxygen (argon group) or 50 vol% nitrogen/50 vol% oxygen (control group) was applied for 1 hour. The primary objective was mortality after subarachnoid hemorrhage. Additionally, outcome was assessed via 1) neurologic testing and 2) an open-field test 24 hours after subarachnoid hemorrhage, 3) protein analysis of hippocampal samples for hypoxia-inducible factor 1α and heme oxygenase 1, and 4) immunohistochemistry of hippocampal slices to quantify vital neurons. Animals were euthanized 6, 24, or 72 hours after subarachnoid hemorrhage or sham surgery. Occurrence of premature death (death prior to scheduled euthanasia) was assessed. Postconditioning with argon resulted in a reduction of risk with respect to premature death to 20.6% compared with the control group (95% CI, 4.39-96.7). Body weight was higher in the argon group over the entire observation period (p < 0.05). There was no difference in the neuroscore (p = 0.550). Expression of hypoxia-inducible factor 1α and heme oxygenase 1 in the hippocampus was increased in the argon group. Higher quantity of vital neurons in the hippocampal samples of the argon group was discovered 24 hours after subarachnoid hemorrhage. Argon application after experimental subarachnoid hemorrhage met the primary endpoint of reducing the risk of mortality. In addition, higher body weight indicating good overall condition was observed in the argon group over the entire observation period. Regarding the mechanism of action, hypoxia-inducible factor 1α-induced heme oxygenase 1 expression resulting in improved survival of neurons may contribute to the beneficial effect of argon application after subarachnoid hemorrhage.

Acute Hypoxic Test in Patients with Prediabetes.

Shatylo, Valerii B., Tetiana V. Serebrovska, Anna V. Gavalko, Egor Egorov, and Oleg V. Korkushko. Acute hypoxic test in patients with prediabetes. High Alt Med Biol. 17:101-107, 2016.-Prediabetes is a state of impaired carbohydrate metabolism when not all of the symptoms required to label a person as diabetic are present, but blood glucose is higher than in healthy subjects. Recent evidence suggests that intermittent hypoxia training (IHT) might provide a cost-effective strategy for improving metabolic functioning. One of the most important aspects of the successful IHT application is individualized approach to hypoxic dose and regimen prescription. To establish the relationships between indices of carbohydrate metabolism and individual resistance to hypoxia, the acute hypoxic test (AHT, breathing gas mixture with 12% O2 during 20 minutes) was performed in 33 healthy volunteers (mean age, 63.0, range, 44-76; fasting plasma glucose (FPG) less than 5.6 mmol/L and 2 hours postoral glucose tolerance test (OGTT) glycemia less than 7.8 mmol/L) and 30 patients with impaired glucose metabolism (mean age, 65.5, range, 44-75; FPG from 5.6 to 6.9 mmol/L and 2 hours post-OGTT glycemia from 7.8 to 11 mmol/L). Negative correlation was found between the SaO2 level at 20th minute AHT and FPG (r = -0.83; p < 0.01) and insulin (r = -0.27; p < 0.05), as well as 2 hours post-OGTT glucose and insulin levels (r = -0.75 and -0.40, respectively). Longer recovery time and less effective functioning of respiratory and cardiovascular systems were also registered in patients with prediabetes showing that their cardiovascular resilience is impaired compared to normoglycemic controls. These patterns of relationship must be considered when assigning the individual modes of IHT.

Relation of retinal blood flow and retinal oxygen extraction during stimulation with diffuse luminance flicker.

Cerebral and retinal blood flow are dependent on local neuronal activity. Several studies quantified the increase in cerebral blood flow and oxygen consumption during activity. In the present study we investigated the relation between changes in retinal blood flow and oxygen extraction during stimulation with diffuse luminance flicker and the influence of breathing gas mixtures with different fractions of O2 (FiO2; 100% 15% and 12%). Twenty-four healthy subjects were included. Retinal blood flow was studied by combining measurement of vessel diameters using the Dynamic Vessel Analyser with measurements of blood velocity using laser Doppler velocimetry. Oxygen saturation was measured using spectroscopic reflectometry and oxygen extraction was calculated. Flicker stimulation increased retinal blood flow (57.7 ± 17.8%) and oxygen extraction (34.6 ± 24.1%; p < 0.001 each). During 100% oxygen breathing the response of retinal blood flow and oxygen extraction was increased (p < 0.01 each). By contrast, breathing gas mixtures with 12% and 15% FiO2 did not alter flicker–induced retinal haemodynamic changes. The present study indicates that at a comparable increase in blood flow the increase in oxygen extraction in the retina is larger than in the brain. During systemic hyperoxia the blood flow and oxygen extraction responses to neural stimulation are augmented. The underlying mechanism is unknown.

ORGANISM REACTION TO DOSED HYPOXIC HYPOXIA IN THE HEALTHY SUBJECTS AND INDIVIDUALS WITH PREDIABETIC HYDROGEN METABOLISM DISTURBANCES.

To assess organism reaction to dosed hypoxic hypoxia in the human invividuals with pre-diabetic hydrogen metabolism disturbances.Altogether 40 subjects, age range 50-74 years, were examined, including 18 persons with pre-diabetic hydrogen metabolism disturbances and 22 essentially healthy subjects. All of them underwent dosed hypoxic test (breathing gas mixture containing 12 % of oxygen during nearly 20 min. The following monitorings were performed: blood saturation (SpO2), breathing rate, arterial blood pressure and heart rate; and standard glucose tolerance test (GTT) for blood plasma glucose and insulin concentration. The patients with prediabetic hydrogen metabolism disturbances displayed a more significant decrease of SpO2 and less effective functioning of the respiratory and cardiovascular systems during dosed hypoxic test compared with the healthy individuals without hydrogen metabolism disturbances. After redistribution of study subjects relative the degree of SpO2 decrease at dosed hypoxic test in the subgroup with satisfactory resistance to hypoxia (subgroup 1: SpO2 more than 80 %) and with reduced (subgroup 2: SpO2 80 % or less) we have found that the fasting glucose level after 2-hour GTT was significantly higher in subgroup 2 versus subgroup 1. The obtained results indicate the interrelationship between organism reaction to hypoxia, in particular between the degree of arterial hypoxemia during performance of the dosed hypoxic test and the indices of fasting glycemia and at standard GTT. The patients with pre-diabetic hydrogen metabolism disturbances are characterized with lower resistance to hypoxic hypoxia.

Dysbarism

Dysbarism is defined as any medical condition that arises as a result of changes in ambient pressure. This review describes dysbarism with a focus on the undersea environment. Conditions discussed in this review include middle and inner ear barotrauma, pulmonary barotrauma, immersion pulmonary edema, decompression illness, and gas toxicities. For each, assessment and stabilization, treatment and disposition, and outcomes are presented. Figures show the AQUARIUS habitat for saturation diving; the anatomy of the external, middle, and inner ear; the Teed classification; the paranasal sinuses; and an example of a recompression chamber. Tables list the types of diving, gas laws relevant to diving, units of underwater pressure, compositions of typical breathing gas mixtures, decompression illness risk factors, symptoms of decompression illness (in order of frequency), signs and symptoms of decompression illness based on body system, maximum recommended depth to reduce the risk of central nervous system oxygen toxicity for various breathing gas mixtures, and progression of nitrogen narcosis symptoms with increasing depth. This review contains 5 highly rendered figures, 9 tables, and 120 references.

The effect of hyperbaric air on the electric activity of neuronal in vitro networks.

Breathing hyperbaric air or gas mixtures, for example during diving or when working underwater is known to alter the electrophysiological behavior of neuronal cells, which may lead to restricted cognition. During the last few decades, only very few studies into hyperbaric effects have been published, especially for the most relevant pressure range of up to 10 bar. We designed a pressurized measuring chamber to record pressure effects on the electrical activity of neuronal networks formed by primary cells of the frontal cortex of NMRI mice. Electrical activity was recorded with multi-electrode arrays (MEAs) of glass neuro chips while subjected to a step-by-step pressure increase from atmospheric pressure (1 bar) to 2 and 4 bar, followed by a decompression to 1 bar, in order to record recovery effects. The effects of pressure on the total spike rates (TSRs), which were averaged from at least 45 chips, were detected in two cell culture media with different compositions. In a DMEM medium with 6% horse serum, the TSR was increased by 19% after a pressure increase to 2 bar and remained stable at 4 bar. In NMEM medium with 2% B27, the TSR was not altered by a pressure increase to 2 bar but increased by 9% at 4 bar. After decompression to 1 bar, the activities decreased to 76% and 101% of their respective control levels in the two media. MEA recordings from neuronal networks in miniaturized hyperbaric measuring chambers provide new access for exploring the neuronal effects of hyperbaric breathing gases.