Preventive Effects And Mechanisms Of Oxygen-increased Respirator On Severe Acute Hypobaric Hypoxia

AIMS: A rabbit simulated acute high altitude (HA) exposure model was established by using an animal decompression chamber, and the study was designed to investigate the preventive effects and potential mechanisms of Oxygen-increased Respirator on severe acute hypobaric hypoxia.METHODS:1. InstrumentOxygen-increased Respirator was invented by Fourth Military Medical University of the Chinese People's Liberation Army. Its work mechanisms is that the partial pressure of oxygen (PO₂) is equal to the total air pressure multiplied by oxygen percentage of the total air ( O₂%), and Oxygen-increased Respirator remains O₂% constant, while increases the total air pressure in Mask by compressing air flow, resulting PO₂ increase. Furthermore, it could significantly increase tidal volume, minute ventilation, gas exchange per minute, and diffusion rate. The whole equipment weighs 370g, takes the size of 152mm×79mm×34mm, its air flow pressurization is 35 mmH₂O achieved by a fan rotating 12 m/s at a air flow of 50 L/min. Its battery can continuously work for more than 10 h and can be recharged for more than 300 times.2. Grouping:Investigate the preventive effects of Oxygen-increased Respirator on severe acute hypobaric hypoxia ( n = 10 each) : Thirty rabbits were randomly divided into three groups: hypobaric hypoxia Group (H), Oxygen-increased Respirator Prevention Group (P) and control(C). Group H were exposed to simulated high altitude of 8500 m for 3 h, and did not wear Oxygen-increased Respirator; Group P were exposed to simulated high altitude of 8500 m for 3 h, and worn Oxygen-increased Respirator. Group C were exposed to normal atmospheric pressure of Xi'an,and did not wear Oxygen-increased Respirator. After the stipulated period of exposure, the animals were quickly sacrificed by removing blood from heart quickly, their related organs water content were measured, their biochemical indexes were determinated, and their histological picture were assessed.3. Observation items:During HA exposure, blood gas analysis was made to observe the changes of PaO₂ and SaO₂. After HA exposure, peripheral vein blood samples were obtained, and lung, brain and myocardium tissues were harvested for further study. Plasma concentrations of TNF-α, D-lactate, LDH, CK, CK-MB, MDA contents, activities of SOD, CAT and GSH-Px were measured respectively. We also detected that lung and brain water contents; NO, MDA contents, activities of SOD, CAT and GSH-Px in lung, brain and myocardium tissues; MPO activities in lung and brain; activities of Na⁺K⁺-ATPase in brain and myocardium tissues and contents of TXB2 and 6-keto-PGF1αin lung tissues.RESULTS:All the values of PaO₂ and SaO₂ in Group P were significantly higher than those in Group H. Group P attenuate the anomalies of following monitored datas and biochemical parameters: the levels of PaO₂ and SaO₂; lung and brain water contents; plasma concentrations of TNF-α, D-lactate, LDH, CK, CK-MB; MDA contents, activities of SOD, CAT and GSH-Px in blood, lung, brain and myocardium tissues; MPO activities in lung and brain; activities of Na⁺ K⁺-ATPase in brain and myocardium tissues and contents of TXB2 and 6-keto-PGF1αin lung tissues.CONCLUSIONS:1. Oxygen-increased Respirator could significantly attenuate acute hypobaric hypoxia-induced oxidative damage, and have the protective effects on lung, brain and myocardium tissues injuries induced by acute hypobaric hypoxia.2. The mechanisms of Oxygen-increased Respirator treatment on acute hypobaric hypoxia induced injury: enhances antioxidase activity and decreases lipid peroxidation damage, regulates releasing rate of vasoconstriction/relaxing factor, decreases inflammatory reaction.