Hyperbarism

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Gerardo Bosco - One of the best experts on this subject based on the ideXlab platform.

  • and hypogravity on skeletal muscle
    2015
    Co-Authors: Gerardo Bosco, Vittore Verratti, Giorgio Fanò
    Abstract:

    Many environmental factors may affect muscle plasticity but some have exclusive characteristics that allow them to play a key role to maintain the muscle capacity to generate force; these factors are: i) the oxygen availability and ii) the load applied to muscle fibres. Hyperbarism is a condition that occurs when a man is subjected to pressure increases. To keep the lungs from collapsing, the air is supplied to him under high pressure which exposes the blood in the lungs to high alveolar gas pressures. Under this condition, the PO2 become sufficiently increased, serious disorders may occur, such as modification of oxygen delivery and/or oxygen availability to permit regular muscle contraction. Also altitude hypobaric hypoxia induces modification of muscle capacity to generate work. Prolonged exposure to high altitude leads significant loss in body mass, thigh muscle mass, muscle fiber area and volume density of muscle mitochondria. Spaceflight results in a number of adaptations to skeletal muscle, including atrophy and early muscle fatigue. Muscle atrophy is observed in a wide range of muscles, with the most extensive loss occurring in the legs, because astronauts are no longer needed to support the body's weight. This review will describe the background on these topics suggesting the strategies to correct the specific muscle changes in presence of environmental stresses, such as the alteration in oxygen-derived signaling pathways or the metabolic consequence of microgravity that may indicate rational interventions to maintain muscle mass and function

  • Hyperbaric Air Exposure at 2.5 ATA Does Not Affect Respiratory Mechanics and Lung Histology in the Rat
    Lung, 2014
    Co-Authors: Alessandro Rubini, Andrea Porzionato, Gloria Sarasin, Susi Zara, Veronica Macchi, Enrico Camporesi, Gerardo Bosco
    Abstract:

    Background We previously demonstrated that the exposure to hyperbaric hyperoxia increased respiratory system elastance and both the “ohmic” and viscoelastic components of inspiratory resistances, probably because of increased oxygen tension toxic effects. We presently investigated the possible consequences of a single exposure to 2.5-atmospheres absolute air (Hyperbarism) lasting 90 min. Methods We used the end-inflation occlusion method on anesthetized rats after about 15 min from previous exposure to Hyperbarism. The method allows the measurements of respiratory system elastance and of the ohmic and viscoelastic components of airway resistance, which respectively depend on the Newtonian pressure dissipation due to the ohmic airway resistance to airflow and on the viscoelastic pressure dissipation caused by respiratory system tissue stress relaxation. The expressions of inducible NO synthase (iNOS) and endothelial NO synthase (eNOS) in the lung’s tissues were also investigated, together with the histological characteristics of lung tissue. Data were compared with those obtained in control animals and in previously studied animals exposed to hyperoxic Hyperbarism. Results Unlike with hyperoxic Hyperbarism, Hyperbarism per se did not change significantly the parameters of respiratory mechanics in the control animals (respiratory system elastance and ohmic and viscoelastic resistances were 2.01 ± 0.17 vs. 1.74 ± 0.08 cm H_2O/ml, and 0.13 ± 0.02 vs. 0.13 ± 0.03 and 0.425 ± 0.04 vs. 0.33 ± 0.03 cm H_2O/ml s^−1 in control vs. experimental animals, respectively, none significantly different), nor did it induce evident effects on lung histology. An increment of both iNOS and eNOS expressions was documented instead (0.50 ± 0.05 vs. 0.75 ± 0.07 and 1.04 ± 0.1 and 1.4 ± 0.15, respectively). Conclusion Our results indicate that, at variance with hyperoxic Hyperbarism, the acute exposure to only Hyperbarism does not affect either the elastic or the resistive respiratory system properties, or lung histology.

  • Hyperbaric air exposure at 2.5 ATA does not affect respiratory mechanics and lung histology in the rat.
    Lung, 2014
    Co-Authors: Alessandro Rubini, Andrea Porzionato, Gloria Sarasin, Susi Zara, Veronica Macchi, Enrico Camporesi, Gerardo Bosco
    Abstract:

    Background We previously demonstrated that the exposure to hyperbaric hyperoxia increased respiratory system elastance and both the “ohmic” and viscoelastic components of inspiratory resistances, probably because of increased oxygen tension toxic effects. We presently investigated the possible consequences of a single exposure to 2.5-atmospheres absolute air (Hyperbarism) lasting 90 min.

  • Performances in extreme environments: effects of hyper/hypobarism and hypogravity on skeletal muscle
    European Journal of Translational Myology, 2010
    Co-Authors: Gerardo Bosco, Vittore Verratti, Giorgio Fanò
    Abstract:

    Many environmental factors may affect muscle plasticity but some have exclusive characteristics that allow them to play a key role to maintain the muscle capacity to generate force; these factors are: i) the oxygen availability and ii) the load applied to muscle fibres. Hyperbarism is a condition that occurs when a man is subjected to pressure increases. To keep the lungs from collapsing, the air is supplied to him under high pressure which exposes the blood in the lungs to high alveolar gas pressures. Under this condition, the PO2 become sufficiently increased, serious disorders may occur, such as modification of oxygen delivery and/or oxygen availability to permit regular muscle contraction. Also altitude hypobaric hypoxia induces modification of muscle capacity to generate work. Prolonged exposure to high altitude leads significant loss in body mass, thigh muscle mass, muscle fiber area and volume density of muscle mitochondria. Spaceflight results in a number of adaptations to skeletal muscle, including atrophy and early muscle fatigue. Muscle atrophy is observed in a wide range of muscles, with the most extensive loss occurring in the legs, because astronauts are no longer needed to support the body's weight. This review will describe the background on these topics suggesting the strategies to correct the specific muscle changes in presence of environmental stresses, such as the alteration in oxygen-derived signaling pathways or the metabolic consequence of microgravity that may indicate rational interventions to maintain muscle mass and function

  • performances in extreme environments effects of hyper hypobarism and hypogravity on skeletal muscle
    European Journal of Translational Myology, 2010
    Co-Authors: Gerardo Bosco, Vittore Verratti, Giorgio Fanò
    Abstract:

    Many environmental factors may affect muscle plasticity but some have exclusive characteristics that allow them to play a key role to maintain the muscle capacity to generate force; these factors are: i) the oxygen availability and ii) the load applied to muscle fibres. Hyperbarism is a condition that occurs when a man is subjected to pressure increases. To keep the lungs from collapsing, the air is supplied to him under high pressure which exposes the blood in the lungs to high alveolar gas pressures. Under this condition, the PO2 become sufficiently increased, serious disorders may occur, such as modification of oxygen delivery and/or oxygen availability to permit regular muscle contraction. Also altitude hypobaric hypoxia induces modification of muscle capacity to generate work. Prolonged exposure to high altitude leads significant loss in body mass, thigh muscle mass, muscle fiber area and volume density of muscle mitochondria. Spaceflight results in a number of adaptations to skeletal muscle, including atrophy and early muscle fatigue. Muscle atrophy is observed in a wide range of muscles, with the most extensive loss occurring in the legs, because astronauts are no longer needed to support the body's weight. This review will describe the background on these topics suggesting the strategies to correct the specific muscle changes in presence of environmental stresses, such as the alteration in oxygen-derived signaling pathways or the metabolic consequence of microgravity that may indicate rational interventions to maintain muscle mass and function.

Alessandro Rubini - One of the best experts on this subject based on the ideXlab platform.

  • Hyperbaric Air Exposure at 2.5 ATA Does Not Affect Respiratory Mechanics and Lung Histology in the Rat
    Lung, 2014
    Co-Authors: Alessandro Rubini, Andrea Porzionato, Gloria Sarasin, Susi Zara, Veronica Macchi, Enrico Camporesi, Gerardo Bosco
    Abstract:

    Background We previously demonstrated that the exposure to hyperbaric hyperoxia increased respiratory system elastance and both the “ohmic” and viscoelastic components of inspiratory resistances, probably because of increased oxygen tension toxic effects. We presently investigated the possible consequences of a single exposure to 2.5-atmospheres absolute air (Hyperbarism) lasting 90 min. Methods We used the end-inflation occlusion method on anesthetized rats after about 15 min from previous exposure to Hyperbarism. The method allows the measurements of respiratory system elastance and of the ohmic and viscoelastic components of airway resistance, which respectively depend on the Newtonian pressure dissipation due to the ohmic airway resistance to airflow and on the viscoelastic pressure dissipation caused by respiratory system tissue stress relaxation. The expressions of inducible NO synthase (iNOS) and endothelial NO synthase (eNOS) in the lung’s tissues were also investigated, together with the histological characteristics of lung tissue. Data were compared with those obtained in control animals and in previously studied animals exposed to hyperoxic Hyperbarism. Results Unlike with hyperoxic Hyperbarism, Hyperbarism per se did not change significantly the parameters of respiratory mechanics in the control animals (respiratory system elastance and ohmic and viscoelastic resistances were 2.01 ± 0.17 vs. 1.74 ± 0.08 cm H_2O/ml, and 0.13 ± 0.02 vs. 0.13 ± 0.03 and 0.425 ± 0.04 vs. 0.33 ± 0.03 cm H_2O/ml s^−1 in control vs. experimental animals, respectively, none significantly different), nor did it induce evident effects on lung histology. An increment of both iNOS and eNOS expressions was documented instead (0.50 ± 0.05 vs. 0.75 ± 0.07 and 1.04 ± 0.1 and 1.4 ± 0.15, respectively). Conclusion Our results indicate that, at variance with hyperoxic Hyperbarism, the acute exposure to only Hyperbarism does not affect either the elastic or the resistive respiratory system properties, or lung histology.

  • Hyperbaric air exposure at 2.5 ATA does not affect respiratory mechanics and lung histology in the rat.
    Lung, 2014
    Co-Authors: Alessandro Rubini, Andrea Porzionato, Gloria Sarasin, Susi Zara, Veronica Macchi, Enrico Camporesi, Gerardo Bosco
    Abstract:

    Background We previously demonstrated that the exposure to hyperbaric hyperoxia increased respiratory system elastance and both the “ohmic” and viscoelastic components of inspiratory resistances, probably because of increased oxygen tension toxic effects. We presently investigated the possible consequences of a single exposure to 2.5-atmospheres absolute air (Hyperbarism) lasting 90 min.

Alessandro Santo - One of the best experts on this subject based on the ideXlab platform.

  • Oxygen-induced retinopathy in the newborn rat: effects of Hyperbarism and topical administration of timolol maleate
    Graefe's Archive for Clinical and Experimental Ophthalmology, 1995
    Co-Authors: Benedetto Ricci, Giuseppe Minicucci, Alessandra Manfredi, Alessandro Santo
    Abstract:

    • Background: Lesions resembling those of human retinopathy of prematurity can be provoked in newborn Wistar rats by exposure to an FiO_2 of 80% for the first 5 days of life followed by 5 days recovery under room-air conditions. • Methods: We evaluated the effects of moderate Hyperbarism (+60.75 kPa, i.e. 455 mmHg or 0.6 atm) and topical administration of 0.25% timolol maleate on oxygen-induced retinopathy (OIR) in this experimental model. • Results: OIR (including neovascularization in most cases) was observed in 100% of the retinas of normobaric oxygen-reared ratlings that did not receive timolol. OIR was less frequent in oxygen-reared ratlings treated with Hyperbarism (60%) or timolol (65%). Hyperbaric oxygen supplementation combined with timolol treatment during both the hyperoxic and room-air phases reduced the incidence of OIR to 30%. There was no sign of vasoproliferation in any of the retinas from the latter three groups. • Conclusions: The highly significant protective effects of Hyperbarism and timolol observed in this study are not fully understood. We speculate that vasoconstriction induced by the Hyperbarism reduces the amount of oxygen that reaches the retina from the choroid during O_2 supplementation, while an increased ocular perfusion pressure caused by timolol-induced reduction of the intraocular pressure might decrease the stimulus to vasoproliferation that normally occurs with room-air recovery.

Badiu G - One of the best experts on this subject based on the ideXlab platform.

Bianca Maria Ricerca - One of the best experts on this subject based on the ideXlab platform.

  • EPO modulation in a 14-days undersea scuba dive.
    International journal of sports medicine, 2013
    Co-Authors: Luca Revelli, Salvatore Vagnoni, Celestino Pio Lombardi, Rodolfo Proietti, Annamaria D'amore, E. Di Stasio, G Storti, Costantino Balestra, Bianca Maria Ricerca
    Abstract:

    Erythropoiesis is affected during deep saturation dives. The mechanism should be related to a downregulation of serum Erythropoietin (s-EPO) concentration or to a toxic effect of the hyperbaric hyperoxia. We evaluated s-EPO and other haematological parameters in 6 scuba divers before, during and after a 14-days guinness saturation dive (8–10 m). Athletes were breathing air at 1.8–2 ATA, under the control of a team of physicians. Serum parameters were measured before diving (T0) and: 7 days (T1), 14 days (T2) after the beginning of the dive and 2 h (T3) and 24 h (T4) after resurfacing. Hgb, and many other haematological parameters did not change whereas Ht, s-EPO, the ratio between s-EPO predicted and that observed and reticulocytes (absolute, percent) declined progressively from T0 to T3. At T4 a significant rise in s-EPO was observed. Hgb did not vary but erythropoiesis seemed to be affected as s-EPO and reticulocyte counts showed. All these changes were statistically significant. The experiment, conducted in realistic conditions of dive length, oxygen concentration and pressure, allows us to formulate some hypotheses about the role of prolonged Hyperbarism on erythropoiesis. The s-EPO rise, 24 h after resurfacing, is clearly documented and related to the “Normobaric Oxygen Paradox”. This evidence suggests interesting hypotheses for new clinical applications such as modulation of s-EPO production and Hgb content triggered by appropriate O 2 administration in pre-surgical patients or in some anemic disease.

  • Erythropoietin Production in Vivo after a Fourteen Days Exposition to Hyperbarism
    Blood, 2008
    Co-Authors: Bianca Maria Ricerca, Salvatore Vagnoni, Anna Maria D’amore, Enrico Di Stasio, Celestino Pio Lombardi, Gabriele Storti, Rodolfo Proietti, Sergio Storti, Luca Revelli
    Abstract:

    Six Italian scuba divers, three men and three women, lived permanently for 14 days at a depth of 8 – 10 metres under the sea level breathing a mixture with the same composition of the air at a pressure ranging between 1,8–2 ATA (Hyperoxic Air-HOA), under the control of a physician’s team. This experience called Abyss project: the “underwater home” was born as a Guinness record attempt, but it had been also surrounded by scientific attention giving the opportunity to collect scientific data. The effect of long-term diving on blood in professional and recreational-professional scuba divers has not been studied. Oxygen is the main regulator of Epo production through the activation or degradation of HIF-1α, the most important transcriptional factor of Epo gene. Hypoxia favours HIF-1α activation, on the contrary hyperoxia favours its degradation. In this case, the excess of Reactive Oxygen Species (ROS), play a crucial role. In the six subjects of Abyss Project, we evaluated S-Epo (Immunoturbidimetric method-Immulite Medical System), CBC and differential (ADVIA 120 Automated Hematology System-Bayer Diagnostics), Reticulocyte count (absolute and perceptual) (Beckman Coulter LH 750-IL Instruments).and the most important hemato-chemical parameters with this timing: before immersion (TIME 0), 7 days (TIME 1), 14 days (TIME 2) after beginning the dive, two hours (TIME 3) and 24 hours (TIME 4) after the resurface. The aim of our study was to investigate if erythropoiesis is affected by a so long diving. Hgb, as far as the hematochemical parameters did not change while Ht, s-Epo, O/P ratio absolute and perceptual reticulocyte counts decline progressively from TIME 0 until TIME 3. At Time 4 (24 hours after the resurface) a rise of Epo production was observed. No significant variation of renal function was registered, According to Repeated Measures ANOVA test, these results are statistically significant (see the Table). We retain that the different results of Hgb and Ht reflect a variation of hydration state. Similar results were obtained previously by other Authors (Balestra C et al J Appl Physiol 2006) although in different experimental conditions and for shorter exposition. Their experiment was conducted in two steps: hyperoxia (100% O2, two hours, with a “nonrebreather” mask) in normobarysm; hyperoxia in hyperbarysm (100% O2, 2,5 ATA, 1,5 hours, in hyperbaric chamber). They observed the rise of s-Epo only 24 hours after the exposition to normobarism, not after the exposition to Hyperbarism. This phenomenon was called “normobaric oxygen paradox”. Our results confirm that the s-Epo production is affected by the exposition to Hyperbarism. It could be hypothesize that the Oxygen dissolved in the plasma influences the s-Epo production, moving the equilibrium between reduction and oxidation towards the last. In fact, no relevant variation of the Hgb Oxygen transport was observed. The reverse of this equilibrium should determine the rise of s-Epo 24 hours after the resurface. Taking in account our results and those of Balestra, it seem that Oxygen pressure, more than O2 concentration, is crucial for the “normobaric oxygen paradox”. Finally, although Hgb did not change, some signs of impairment of erythropoiesis are already present. In fact, absolute and perceptual reticulocyte counts decline from Time 0 to time 4. Taking into account the timing of erythropoiesis, it is predictable that anemia would be a clinical problem if the exposition continued. In fact, erythropoiesis could suffer from the Epo reduction and also from the enhancement of the apoptosis. The last effect could be produced either by the Epo reduction, either by a direct effect of hyperoxia as demonstrated in vitro (Ganguly BJ Apoptosis 2002). | T | Hgb g/dl | Ht | Ret% | Ret 10^9/l | s-Epo mU/ml | |:-:| ---------- | ---------- | --------- | ----------- | ----------- | | | 14,03±1,25 | 41,32±2,81 | 1,19±0,35 | 56,40±22,09 | 11,58±3,09 | | 1 | 13,72±1,39 | 40,03±3,37 | 1,08±0,50 | 50,72±26,16 | 6,28±3,20 | | 2 | 13,33±1,80 | 38,83±4,35 | 0,72±0,23 | 32,58±12,82 | 4,23±1,59 | | 3 | 13,40±1,43 | 39,77±3,38 | 0,67±0,17 | 30,18±8,90 | 4,50±1,73 | | 4 | 13,67±1,35 | 39,82±3,43 | 0,71±0,28 | 32,96±13,44 | 14,02±5.05 | | P | n.s. |