This paper describes electrostatic harms to oxygen pressure cabins and protection measures which should be taken.
Fires ; prevention & control ; Humans ; Humidity ; Hyperbaric Oxygenation ; Oxygen Inhalation Therapy ; instrumentation ; Static Electricity ; adverse effects

This paper introduces a kind of union of hyperbaric oxygen-cabins and a microcomputer through which, the temperature measurement, the monitoring of oxygen concentration and air exchange are realized automatically with uniformly ascending voltage and static constant voltage.
Automatic Data Processing ; Equipment Design ; Humans ; Hyperbaric Oxygenation ; instrumentation ; Microcomputers ; Oxygen Inhalation Therapy ; instrumentation ; Software

OBJECTIVETo observe the therapic effects of the recompression treatment schedule D2 (breathing 100% oxygen at 0.12 MPa gauge pressure) on the type I decompression illness (DCI) by hyperbaric chamber pressurized with air.

METHODSThe recompression treatment schedule D2 was from the decompression treatment tables of in Germany BGI690. Seven cases on work site group (work site group) and five cases in hospital (hospital group) were treated using recompression treatment. All cases suffered from type I DCI after normal decompression procedures from working in compressed air in tunnel construction. These patients were treated with basic schedule D2 or extended schedule D2 according to the symptoms of the cases responded to recompression therapy.

RESULTSIn the work site group, the pains of joints, arms and legs were released quickly, the therapic effects appeared at (8.1 +/- 8.1) min, the cases were cured with a recompression therapy of basic schedule D2, the total mean time of treatment was (150 +/- 0.0) min. In the hospital group, the pains of joints, arms and legs disappeared slowly, the therapic effects appeared at (115.0 +/- 60.0) min, the cases were cured with a recompression therapy of extended schedule D2, the total mean time of treatment was (270.0 +/- 0.0) min, which was significantly longer than that in the work site group (P<0.01).

CONCLUSIONSThe treatment pressure is 0.12 MPa(gauge pressure) in schedule D2 with medical hyperbaric chamber pressurized with air,which can be used for treatment of type I DCI, the curative effects in the work site group are better than those in the hospital group.

Adult ; Decompression ; methods ; Decompression Sickness ; therapy ; Diving ; Humans ; Hyperbaric Oxygenation ; methods ; Male ; Middle Aged ; Oxygen Inhalation Therapy ; Treatment Outcome

OBJECTIVETo study therapeutic effects by using different oxygen therapies in rats with acute carbon dioxide poisoning, to select the best oxygen therapy technology for patients with acute carbon dioxide poisoning on the spot.

METHODSSixty healthy male Sprague-Dawley rats were randomized into normal control group, carbon dioxide exposure group, hyperbaric oxygen treatment group (pressure 2 ATA, FiO(2)100%), high concentration of atmospheric oxygen treatment group (FiO(2)50%), low concentration of atmospheric oxygen treatment group (FiO(2)33%). After treated with different oxygen in rats with acute carbon dioxide poisoning, arterial pH, PO2 and PCO2 of rats were detected, in addition observe pathological changes of lung tissue and brain tissue.

RESULTSThe arterial pH (7.31 ± 0.06) and PO2 [(68.50 ± 15.02) mm Hg] of carbon dioxide exposure group were lower than those of control group [pH (7.42 ± 0.02) and PO2 (92.83 ± 8.27) mm Hg], PCO2 [(71.66 ± 12.10) mm Hg] was higher than that of control group [(48.25 ± 2.59) mm Hg] (P < 0.05); the arterial pH (hyperbaric oxygen treatment group 7.37 ± 0.02, high concentration of atmospheric oxygen treatment group 7.39 ± 0.03, low concentration of atmospheric oxygen treatment group 7.38 ± 0.02) and PO2 of oxygen treatment groups [hyperbaric oxygen treatment group, high concentration of atmospheric oxygen treatment group, low concentration of atmospheric oxygen treatment group were (82.25 ± 12.98), (84.75 ± 11.24), (83.75 ± 16.77) mm Hg, respectively] were higher than that of carbon dioxide exposure group, PCO2 [hyperbaric oxygen treatment group, high concentration of atmospheric oxygen treatment group, low concentration of atmospheric oxygen treatment group were (52.25 ± 4.95), (51.75 ± 4.82), (52.66 ± 5.61) mm Hg, respectively] was lower than that of carbon dioxide exposure group (P < 0.05); there was no significant difference of the arterial pH, PO2 and PCO2 between oxygen treatment groups and control group (P > 0.05); there was no significant difference of the arterial pH, PO2 and PCO2 among oxygen treatment groups (P > 0.05). There was large area of bleeding of lungs in rats with carbon dioxide poisoning, the bleeding of lungs in rats with high concentration of atmospheric oxygen treatment and low concentration of atmospheric oxygen treatment was better than the rats with carbon dioxide poisoning, there was no abnormal appearance of lungs in rats with hyperbaric oxygen treatment. The light microscope observation showed that there were diffuse bleeding and exudation of lungs in rats with carbon dioxide poisoning, the bleeding and exudation of lungs in rats with high concentration of atmospheric oxygen treatment and low concentration of atmospheric oxygen treatment were better than the rats with carbon dioxide poisoning, there were only minor bleeding and exudation of lungs in rats with hyperbaric oxygen treatment. There was no difference of brain in anatomy and microscopy among all groups, there were no significant bleeding, edema, cell degeneration and necrosis.

CONCLUSIONSLung pathology in acute carbon dioxide poisoning rats with hyperbaric oxygen treatment is better than the rats with high concentration of atmospheric oxygen treatment and low concentration of atmospheric oxygen treatment, there is no significant difference of effect between high concentration of atmospheric oxygen treatment group and low concentration of atmospheric oxygen treatment group, however, the results of blood gas analysis and lung pathology than the exposure group improved, so qualified medical unit for hyperbaric oxygen therapy as soon as possible, hyperbaric oxygen treatment facilities in the absence of circumstances, the emergency treatment of early oxygen is also a good measure.

Animals ; Carbon Dioxide ; poisoning ; Hyperbaric Oxygenation ; Lung ; pathology ; Male ; Oxygen Inhalation Therapy ; methods ; Rats ; Rats, Sprague-Dawley ; Treatment Outcome

OBJECTIVETo Evaluate the effects of different oxygen therapies on the rats with acute nitrogen asphyxia and to study the best oxygen therapic protocol for patients with acute nitrogen asphyxia on the spot.

METHODSSixty healthy male Wistar rats were divided into 5 groups: control, exposure to nitrogen, 33% oxygen treatment, 50% oxygen treatment and hyperbaric oxygen treatment groups. The behavioral performance, arterial oxygen pressure (PO2), carbon dioxide partial pressure (PCO2) and oxygen saturation (SPO2), biochemical changes in liver and kidney function and myocardial enzymes in 5 groups were measured.

RESULTSThe rats exposed to nitrogen firstly were excited then inactive symptoms, but consciousness was recovered after oxygen therapy. The PO2 and SPO2 in nitrogen exposure group were (79.67 +/- 9.12) and (94.92 +/- 2.78) mm Hg, respectively, which were significantly lower than those in control group (P<0.01). The PO2 and SPO2 of 3 oxygen treatment groups were (94.75 +/- 7.24), (94.92 +/- 8.98), (104.58 +/- 7.12)mm Hg and (97.17 +/- 0.83), (96.92 +/- 1.16), (97.42 +/- 0.67)mm Hg, respectively, which were significantly higher than those in nitrogen exposure group (P<0.05). The PO2 in hyperbaric oxygen treatment group was significantly higher than those in other 2 oxygen treatment groups (P<0.05). The SPO2 in hyperbaric oxygen treatment group was (51.42 +/- 6.60) mm Hg which was significantly higher than that [(44.58 +/- 3.42)mm Hg] in 50% oxygen treatment groups (P< 0.05). AST [(270.50 +/- 49.05 )U/L], ALT [(122.67 +/- 55.44 )U/L], BUN [(7.31 +/- 0.93 )mmol/L], Cr[(28.32 +/- 4.35) micromol/L], CK [(1808.42 +/- 582.05)U/L] and CtnI [(22.52 +/- 14.29 )ng/ml] in nitrogen exposure group were significantly higher than those in control group (P<0.05). AST [(165.25 +/- 30.87) U/L], HBDH [(350.83 +/- 103.00)U/L] and CtnI [(11.23 +/- 5.38) ng/ml] in hyperbaric oxygen treatment group were significantly lower than those in other 2 oxygen treatment groups (P<0.05).

CONCLUSIONTimely and effective oxygen therapy can significantly increase arterial pressure of oxygen and oxygen saturation in the rats with acute nitrogen asphyxia, and can improve liver function and cardiac damage. The hyperbaric oxygen chamber can significantly increase the therapeutic effects on rats with acute nitrogen asphyxiation.

Animals ; Asphyxia ; blood ; chemically induced ; Blood Gas Analysis ; Hyperbaric Oxygenation ; Male ; Nitrogen ; toxicity ; Oxygen Inhalation Therapy ; Rats ; Rats, Wistar

OBJECTIVETo evaluate the effects of different oxygen therapy technique (different concentrations of normobaric oxygen and the hyperbaric oxygen) on the ultrastructure of cardiac muscle, lung and liver in rats with acute hydrogen sulfide intoxication.

METHODSOne hundred healthy male Wistar rats were randomly divided into five groups: normal control group (A), poisoned group (B), oxygen therapy group (C), oxygen therapy group (D) and oxygen therapy group (E). After the exposure to 300 ppm H2S for 60 min in a static exposure tank (1 m3), the rats were treated with oxygen therapy, C, D and E groups were given 33% oxygen, 50% oxygen of atmospheric oxygen and hyperbaric oxygen therapy for 100 min, respectively. The rats in normal control group inhaled air under the same environment. After exposure and therapy, the tissues of lung, heart and liver were observed under light microscope and electron microscope.

RESULTSThe results of light microscope examination showed that the broken and not well aligned cardiac myofilaments, cytoplasmic edema and pyknosis could be seen in group B. The well aligned and clear cardiac myofilaments appeared in group C, D and E. The alveolar hemorrhage, edema and inflammatory cells exudation could not be seen in group A. Alveolar epithelial cell edema, unsmooth alveolar edge and alveolar inflammatory cells exudation could be found in group B. The unsmooth alveolar septal borders and pulmonary edema could be seen occasionally in group C and D, the alveolar inflammatory cells exudation could not be seen in group E. The regular hepatic boards and the uniform hepatic cellular nuclei were found in group A. The disordered hepatic boards, widened cellular gaps and cytoplasmic edema could be seen occasionally in group B. The irregular hepatic boards and ballooning degeneration could be seen in group C and D. The regular hepatic boards and uniform cytoplasm could be found in group E. The results of electron microscope examination indicated that the mitochondrial swelling, autolyzing, fuzzy and breakage of myocardial cells were observed in group B; the clear mitochondrial structure appeared in group E. The apoptosis and organelle vacuole of alveolar epithelial cells could be observed in group B. The relatively normal nuclei of alveolar epithelial cells could be seen in group E. The lax cytoplast structure of hepatocytes, unclear nuclear membrane, lumped chromatin, slightly swelled mitochondria and phagosomes were observed in group B. However, no improved change was observed in group C, D and E.

CONCLUSIONHydrogen sulfide could induce the extensive and severe damage of myocardial mitochondria, alveolar epithelial cells and hepatocytes, the oxygen therapy in good time could reduce significantly the myocardial injury, and improve the lung injury to some extent. High-pressure oxygen therapy is better than the normobaric oxygen therapy.

Animals ; Hydrogen Sulfide ; poisoning ; Hyperbaric Oxygenation ; Liver ; pathology ; Lung ; pathology ; Male ; Myocardium ; pathology ; Oxygen Inhalation Therapy ; Pulmonary Alveoli ; pathology ; Rats ; Rats, Wistar

This paper introduces a self-made intelligent oxygen-inhalation accumulative calculagraph. A photoelectric probe is fixed on the buoy of the oxygen flowmeter under non-ventilation conditions.When the oxygen flowmeter is switch on, the buoy floats up, the oxygen supply begins and the timing starts at the same time. When oxygen inhalation pauses, the buoy goes down and the timing stops. When oxygen inhalation starts again, the timing continues and accumulates.
Artificial Intelligence ; Oxygen Inhalation Therapy ; instrumentation

This paper analyses the defects of bubble oxygen inhalators currently used, and investigates into their solutions for improvement.
Oxygen Inhalation Therapy ; instrumentation ; methods ; Oxygenators ; standards

No abstract available.
Catheters* ; Humans ; Oxygen Inhalation Therapy ; Oxygen* ; Thrombotic Microangiopathies*

No abstract available.
Catheters* ; Humans ; Oxygen Inhalation Therapy ; Oxygen* ; Thrombotic Microangiopathies*