Fig 4 - uploaded by Noemi Bitterman
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Day to day variations in time duration until onset of CNS oxygen toxicity symptoms of a single diver. From Donald, 1947 (16).
Source publication
This chapter will present our current knowledge on the major toxic manifestations of oxygen; the clinical features-descriptions
and incidence of symptoms, mechanisms underlying the oxidative insult, the time-duration relationship defining the safety
limits, risk factors leading to enhanced toxicity, and strategies for protection
Context in source publication
Context 1
... rhythm (29), various drugs, age (30), sex (31), interspecies differences and individual day to day variability (16) may contribute to the sensitivity to CNS oxygen toxicity (14). Figure 4 presents data from a unique study by Donald in 1947, in which he exposed a single diver to the same profile of HBO 2 for twenty times within a three month period, until the appearance of neurological symptoms of oxygen toxicity (16). As can be seen, there are large day to day variations in time duration of symptoms, suggesting that there is no fixed, personal, predetermined threshold of tolerance to oxygen toxicity. ...
Citations
... Animal experiments have indicated a variation in tolerance similar to that found in central nervous system toxicity between different species. For O 2 partial pressure levels <0.3 bar, humans are not harmed by O 2 at all, but for >0.5 bar pulmonary toxicity symptoms set in (e.g., Clark and Lambertsen, 1971); O 2 partial pressures of 1 bar and more cause irreversible damage (Bitterman and Bitterman, 2006). In addition, O 3 can be toxic to animal-like life in high concentrations (>40 ppb) at a planet's surface (Cooke et al., 2024), even though it is an important UV absorber at high altitudes. ...
In this hypothesis article, we discuss the basic requirements of planetary environments where aerobe organisms can grow and survive, including atmospheric limitations of millimeter-to-meter-sized biological animal life based on physical limits and O2, N2, and CO2 toxicity levels. By assuming that animal-like extraterrestrial organisms adhere to similar limits, we define Earth-like habitats (EH) as rocky exoplanets in the habitable zone for complex life that host N2-O2-dominated atmospheres with minor amounts of CO2, at which advanced animal-like life or potentially even extraterrestrial intelligent life can in principle evolve and exist. We then derive a new formula that can be used to estimate the maximum occurrence rate of such Earth-like habitats in the Galaxy. This contains realistic probabilistic arguments that can be fine-tuned and constrained by atmospheric characterization with future space and ground-based telescopes. As an example, we briefly discuss two specific requirements feeding into our new formula that, although not quantifiable at present, will become scientifically quantifiable in the upcoming decades due to future observations of exoplanets and their atmospheres. Key Words: Eta-Earth-Earth-like habitats-oxygenation time-nitrogen atmospheres-carbon dioxide-animal-like life. Astrobiology 24, 897-915.
... Regardless, recent and ongoing research is testing the effectiveness of certain key physiological responses as predictors of an impending seizure; that is, so-called "physio-markers" for early warning of a toxic CNS-OT hit. Potential physio-markers include hyperoxic hyperpnea/hyperventilation [69,152], heart rate and pattern [122,158], hyperoxic hypothermia [93,155,165], and possibly other predictors [20,86,191]. ...
... Additional important risk factors that accelerate onset of CNS-OT are exercise, immersion, and cold [20,86,191]. As stated, exercise increases end-tidal CO 2 with the consequences just listed above. ...
Hyperbaric oxygen (HBO 2 ) is breathed during hyperbaric oxygen therapy and during certain undersea pursuits in diving and submarine operations. What limits exposure to HBO 2 in these situations is the acute onset of central nervous system oxygen toxicity (CNS-OT) following a latent period of safe oxygen breathing. CNS-OT presents as various non-convulsive signs and symptoms, many of which appear to be of brainstem origin involving cranial nerve nuclei and autonomic and cardiorespiratory centers, which ultimately spread to higher cortical centers and terminate as generalized tonic-clonic seizures. The initial safe latent period makes the use of HBO 2 practical in hyperbaric and undersea medicine; however, the latent period is highly variable between individuals and within the same individual on different days, making it difficult to predict onset of toxic indications. Consequently, currently accepted guidelines for safe HBO 2 exposure are highly conservative. This review examines the disorder of CNS-OT and summarizes current ideas on its underlying pathophysiology, including specific areas of the CNS and fundamental neural and redox signaling mechanisms that are thought to be involved in seizure genesis and propagation. In addition, conditions that accelerate the onset of seizures are discussed, as are current mitigation strategies under investigation for neuroprotection against redox stress while breathing HBO 2 that extend the latent period, thus enabling safer and longer exposures for diving and medical therapies.
Objective
Closer monitoring and treatment is vital for pregnant carbon monoxide (CO) poisoning cases due to fetal poisoning component. Permanent damage can occur in both the mother and the baby. It may cause stillbirth even though no serious clinical symptoms occur in the mother. Hyperbaric oxygen (HBO) treatment is advised for all pregnant patients regardless of their clinical symptoms. Pregnant CO poisoning patients that received HBO treatment and their fetal status were evaluated in this study.
Methods
Pregnant patients poisoned with CO treated in the same hyperbaric clinic were evaluated. Pregnant patients that received HBO treatment in a multiplace chamber were evaluated in terms of clinical status, demographic structure, laboratory tests, fetal effects and progress of the fetus until birth and 6 months postpartum.
Results
A total number of 32 pregnant cases were treated. COHb values were over 20% (min 6.9- max 40.2) in 23 patients, 11 patients had a history of syncope. All patients took HBO treatment under 2.4 ATA pressure for 120 min. 3 patients received more than 1 session of HBO treatments due to fetal stress; all other cases took 1 session of HBO treatment. No spontaneous abortus occurred in early follow-ups; only 4 babies were born prematurely. 2 of the babies were lost in the early phases after birth, due to causes non-related to CO poisoning complications (cyanotic heart disease, necrotising enterocolitis). No significant difference were observed in the comparison of laboratory results of patients with syncope and of those who did not have syncope and comparison of patients with COHb value higher than 20% and patients with COHb value lower than 20% (p > 0.05).
Conclusion
HBO is not advisable for pregnant patients except for CO poisoning. In this study it is observed that HBO treatment under 2.4 ATA pressure for 120 min has no harmful effects on the mother and the fetus. It is observed that continuation of HBO treatment in the cases with fetal distress findings has beneficial effects. COHb levels and syncope were shown to have no significant effect on clinical symptoms and on blood tests.
Abnormally shaped red blood cells (RBCs), called poikilocytes, can cause anemia. At present, the biochemical abnormalities in poikilocytes are not well understood. Normal RBCs and poikilocytes were analyzed using whole-blood and single-cell methods. Poikilocytes were induced in rat blood by intragastrically administering titanium dioxide (TiO2) nanoparticles. Complete blood count and inductively coupled plasma mass spectrometry analyses were performed on whole-blood to measure average RBC morphology, blood hemoglobin (HGB), iron content, and other blood parameters. Follow-up confocal Raman spectroscopy was performed on single RBCs to analyze cell-type-specific HGB content. Two types of poikilocytes, acanthocytes and echinocytes, were observed in TiO2 blood samples, along with normal RBCs. Acanthocytes (diameter 7.7 ± 0.5 μm) and echinocytes (7.6 ± 0.6 μm) were microscopically larger (p < 0.05) than normal RBCs (6.6 ± 0.4 μm) found in control blood samples (no TiO2 administration). Similarly, mean corpuscular volume was higher (p < 0.05) in TiO2 whole-blood (70.70 ± 1.97 fl) than in control whole-blood (67.42 ± 2.03 fl). Poikilocytes also had higher HGB content. Mean corpuscular hemoglobin was higher (p < 0.05) in TiO2 whole-blood (21.84 ± 0.75 pg) than in control whole-blood (20.8 ± 0.32 pg). Iron content was higher (p < 0.001) in TiO2 whole-blood (697.0 ± 24.5 mg / l) than in control whole-blood (503.4 ± 38.5 mg / l), which supports elevated HGB as iron is found in HGB. HGB-associated Raman bands at 1637, 1585, and 1372 cm - 1 had higher (p < 0.001) amplitudes in acanthocytes and echinocytes than in RBCs from control blood and normal RBCs from TiO2 blood. Further, the 1585-cm - 1 band had a lower (p < 0.05) amplitude in normal RBCs from TiO2 versus control RBCs. This represents biochemical abnormalities in normal appearing RBCs. Overall, poikilocytes, especially acanthocytes, have elevated HGB.
Objective: Hyperbaric oxygen treatment is based on breathing pure oxygen under pressure higher than the ambient pressure. Signs of toxicity can occur due to the presence of oxygen and nitrogen reactive substances during exposure to high doses of oxygen. Aim of study: To find the incidence of oxygen toxicity in patients treated in our centre in 1994-2005. Design: Observational retrospective study. Results: 4,164 patients underwent total 48,992 treatment sessions in the period studied. Thirteen cases of toxicity occurred in 7 patients. The most dramatic symptom of oxygen CNS toxicity - hyperoxia-induced seizures - were observed in 4 patients (0.008%). The relation between hyperoxia-induced seizures and treatment pressure at different time periods was analysed and compared with the results of our previous study from 1984. Conclusion: Hyperbaric oxygen treatment is a safe and well tolerated method with a low incidence of CNS toxicity. The incidence of hyperoxia-induced seizures presented in our paper is almost the lowest of recently published studies. No injury or permanent sequelae were observed in relation to hyperoxia-induced seizures.
A non-healing wound is defined as showing no measurable signs of healing for at least 30 consecutive treatments with standard wound care.[1] It is a snapshot of a patient's total health as well as the ongoing battle between noxious factors and the restoration of optimal macro and micro circulation, oxygenation and nutrition. In practice, standard therapies for non-healing cutaneous wounds include application of appropriate dressings, periodic debridement and eliminating causative factors.[2] The vast majority of wounds would heal by such approach with variable degrees of residual morbidity, disability and even mortality. Globally, beyond the above therapies, newer tools of healing are selectively accessible to caregivers, for various logistical or financial reasons. Our review will focus on the use of hyperbaric oxygen therapy (HBOT), as used at our institution (CAMC), and some other modalities that are relatively accessible to patients. HBOT is a relatively safe and technologically simpler way to deliver care worldwide. However, the expense for including HBOT as standard of care for recognized indications per UHMS(Undersea and Hyperbaric Medical Society) may vary widely from country to country and payment system.[3] In the USA, CMS (Centers for Medicare and Medicaid Services) approved indications for HBOT vary from that of the UHMS for logistical reasons.[1] We shall also briefly look into other newer therapies per current clinical usage and general acceptance by the medical community. Admittedly, there would be other novel tools with variable success in wound healing worldwide, but it would be difficult to include all in this treatise.
Diving renders negative influence on human respiratory system especially when oxygen breathing apparatus aimed for military divers is used. Spirometry indexes have poor sensitivity to toxic effect of hyperbaric hyperoxia. Objective is to develop new acoustic instrumentation for revealing minimum impairments of lung function in oxygen divers. The apparatus has been designed which is based on analysis of forced expiratory tracheal noise duration (FETND). This apparatus contains acoustic sensor, input device, portable personal computer and specially designed software. 48 divers before and after single shallow water dive in oxygen closed-type breathing apparatus were tested by means of this acoustic tool. After dive a significant drop of spirometric indexes forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1) over the group as a whole was found. The significant increase of individual FETND, exceeding the natural variability limit, was found in 10 subjects (20.8%). Three of them during dive had respiratory symptoms characteristic for initial manifestations of pulmonary oxygen poisoning. Two of them had essential drop of FEV1. The asymptomatic reversible increase of FETND in the rest 7 divers was interpreted as a sign of obstructive impairments caused by hidden phase of hyperbaric hyperoxia effect. Thus developed acoustic tool is useful to monitor ventilation function of lungs in military/civil divers and other persons working in harmful gas media such as firefighters, astronauts and so on.
Decreased availability of oxygen to metabolizing cells is a major feature of circulatory shock that leads to tissue damage and multiple organ dysfunctions. A wish to alleviate tissue hypoxia underlies the common clinical use of hyperoxic ventilation in shock. Yet, this straightforward approach is met by skepticism that is based on the potential pro-inflammatory effects of hyperoxia and the acknowledged roles of reactive oxygen species and oxidative stress in tissue injury. A steadily growing body of experimental data indicates that hyperoxia exerts an extensive profile of physiologic and pharmacologic effects that improve tissue oxygenation, exert anti-inflammatory and antibacterial effects, augment tissue repair mechanisms, and may also decrease oxidative stress during shock. The currently available preclinical information on the benefits of early use of safe regimens of hyperoxic ventilation alone or in combination with other commonly employed modalities sets the stage for renewal of careful clinical evaluation of oxygen therapy in resuscitation of circulatory shock.
We evaluated the effects of hyperoxia on pulmonary inflammatory changes in sepsis induced by cecal ligation and puncture (CLP) in rats. Seven groups were studied: sham-operated rats breathing air for 20 or 48 h; CLP breathing air for 20 or 48 h; and CLP + 100% oxygen for 20 h, or 70% oxygen for 48 h, or 100% oxygen intermittently (6 h/d) for 48 h. Video microscopy was used to monitor lung macromolecular leak, microvascular flow velocity, and shear rates, and lung morphometry was used for leukocyte infiltration and solid tissue area. Cell counts, tumor necrosis factor α, and nitrites were determined in peripheral blood and lung lavage fluid. Expression of adhesion molecules in blood leukocytes was evaluated by flow cytometry. Cecal ligation and puncture induced inflammation manifested in leukopenia, left shift, thrombocytopenia, increased expression of L selectin and CD11, increased serum and lavage fluid tumor necrosis factor α and leukocytes, and increased lung tissue area, macromolecular leak, and sequestration of leukocytes. Inhalation of 100% oxygen for 20 h increased nitrites (P < 0.01) and decreased leukocyte count in lavage fluid (P < 0.05) and attenuated lung macromolecular leak and changes in solid tissue area (P < 0.01). Inhalation of 70% oxygen (48 h) attenuated expression of adhesion molecules (P < 0.001) but failed to attenuate markers of lung inflammation. In contrast, intermittent 100% oxygen exerted favorable effects on markers of inflammation, attenuated leukocyte expression of L selectin and CD11 (P < 0.01), decreased pulmonary sequestration of leukocytes (P < 0.001), and ameliorated changes in macromolecular leak (P < 0.01) and lung solid tissue area (P < 0.05). Our data support the beneficial effects of safe subtoxic regimens of normobaric hyperoxia on the systemic and pulmonary inflammatory response following CLP.
