Effect of different pressure oxygen pre-breathe in diving decompression sickness of rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the effect of different pressure oxygen pre-breathing in preventing decompression sickness of rats.</p><p><b>METHODS</b>Forty male SD rats were randomly divided into 4 groups: decompression sickness (DCS) group and three oxygen pre-breathing groups with 1 ATA, 2 ATA and 3 ATA pressure respectively. The rats of DCS group were placed in the hyperbaric chamber and the chamber was compressed evenly within 3 minutes to depths of 7 absolute atmosphere(ATA) and held at the designated depth for 60 min, then decompressed (3 min) at constant speed to the surface pressure. After that, the rats were taken out for further detection. While the rats of oxygen pretreatment groups pre-breathed different pressure oxygen for 20 min before entering into chamber. The mortality and behavioral of rats were observed with 30 min post decompression. The dry/wet ratio of the lung, protein levels in the bronchoalveolar lavage fluid (BALF), and the inflammatory cytokine tumor necrosis factor (TNF-alpha) expression were also tested.</p><p><b>RESULTS</b>Compared with that of the DCS group, the mortality and morbidity of oxygen pre-breathe groups didn't change obviously. But the total BALF protein level and the inflammatory cytokine TNF-alpha expression of 1 ATA oxygen pre-breathe group were obviously decreased, while the dry/wet ratio of lung as obviously increased instead (P < 0.05).</p><p><b>CONCLUSION</b>Although preoxygenation can' t obviously change the mortality and mobidity of rats, normal pressure oxygen pre-breathing can mitigate the protein infiltration in BALF and the expression of inflammatory cytokine in lung tissue.</p>

The change of NOS in pulmonary oxygen toxicity induced by different oxygen pressure / 中国应用生理学杂志

<p><b>OBJECTIVE</b>Long time exhaled oxygen will induced oxygen toxicity. Some studies had found that different pathology may exised in normobaric and hyperbaric pulmonary oxygen toxicity, and nitric oxide synthase (NOS) may play a role. In this study, we discussed the change of NOS in normobaric and hyperbaric pulmonary oxygen toxicity.</p><p><b>METHODS</b>Sixty male SD rats were randomly divided into 6 groups (n = 10), exposed to 1 ATA (atmosphere absolute), 1.5 ATA, 2 ATA, 2.5 ATA and 3 ATA, 100% oxygen for 56, 20, 10, 8, 6 hours respectively. Rats were exposed to air as control. After exposure, the protein in bronchoalveolar lavage fluid (BALF), the wet/dry weight of lung and the expression of eNOS, nNOS in lung were defined.</p><p><b>RESULTS</b>As compared to air group, the protein in BALF, the wet/dry of lung were significantly elevated in 1.0 ATA group, while these changes were not so obviously in the other groups, and these changes in hyperbaric oxygen group (approximately 1.0 ATA) were significantly decreased as compared with nonnrmobaric oxygen group (1.0 ATA). The expression of nNOS were not changed in normobaric and hyperbaric pulmonary oxygen toxicity, while the expression of eNOS was significantly decreased in 2 ATA group, and significantly elevated in 2.5 ATA and 3 ATA group.</p><p><b>CONCLUSION</b>The expression of eNOS can change when exposed to different pressures of oxygen.</p>

Change of adhesion molecules in the lungs of rat with decompression sickness / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the change of adhesion molecules in the lungs of rats suffered with decompression sickness (DCS).</p><p><b>METHODS</b>Male SD rats were placed in the hyperbaric chamber, the chamber was compressed within 3 minutes to depths of 7 absolute atmosphere (ATA) and held at the designated depth for 60 min, then rapidly decompressed (3 min) to the surface. Rats were observed for signs of DCS after decompression. The brains, hepatis, and lungs were removed at 30 min, 6 h, 24 h post decompression, fixed and stained with hematoxylin eosin for routine histologic analysis. Lung paraffin sections were immunostained for the expression of intercellular adhesion molecule-1 (ICAM-1), E-selectin and major histocompatibility complex class II molecule (MHC-II). 2% evans blue dye in normal saline was injected 30 minutes prior to 6 h, 24 h before decompression. After 30 min, animals were perfused with 0.9% normal saline and lungs were harvested. Evans blue in the plasma was quantified by wavelength spectrophotometric analysis at 620 nm.</p><p><b>RESULTS</b>Results showed that there were hemorrhage and edema changes in the lungs, liver and brain at 30 min post decompression. Compared with control animals maintained at 1 ATA, the levels of E-selectin, ICAM-1 and MHC-II in the lungs of DCS rats were significantly increased post decompression. Compared with control animals, evans blue in the plasma was much higher at 6 h, 24 h post decompression.</p><p><b>CONCLUSION</b>The bubble-induced adhesion molecule-mediated endothelial activation may be involved in the pathogenesis of DCS.</p>

The research progress of diving medicine in China / 中国应用生理学杂志

Diving medicine is one of the branches of military medicine, and plays an important role in naval development. This review introduces the progress of researches on undersea and hyperbaric physiology and medicine in the past few years in China. The article describes our research achievement in conventional diving and its medical support, researches on saturation diving and its medical support, submarine escape and its medical support, effects of hyperbaric environments and fast buoyancy ascent on immunological and cardiological functions. Diving disorders (including decompression sickness and oxygen toxicity) are also introduced.

Effect of hyperbaric oxygen on the expression of nitric oxide synthase mRNA in cortex after acute traumatic cerebral injury / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the effect of hyperbaric oxygen (HBO) treatment on the expression of nitric oxide synthase (NOS) mRNA in cortex after acute traumatic cerebral injury, and to study the mechanism of HBO on brain injury.</p><p><b>METHODS</b>Acute traumatic brain injury model was established with rest received free fall injury method in SD rats. 0.25 MPa HBO treatment was used 1 h or 12 h after brain injury and the cortex was isolated 6 h or 24 h after brain injury respectively. The expression of mRNA coding for nNOS, eNOS or iNOS were assayed using reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>The expression of nNOS, eNOS and iNOS mRNA were significantly decreased in 0.25 MPa HBO treatment groups than those in acute cerebral injury groups (P < 0.01). The amount of nNOS, eNOS and iNOS mRNA was significantly lower in HBOT 24 h group than those in HBOT 6 h group (P < 0.05, P < 0.01). There was no significantly difference among nNOS, eNOS and iNOS mRNA in 0.25 MPa normoxic hyperbaric nitrogen groups and acute cerebral injury groups (P > 0.05).</p><p><b>CONCLUSION</b>HBO may exert significant effects on the expression of nNOS mRNA/iNOS mRNA and protect cortical neuronal from traumatic cerebral injury.</p>

The variation of PPAR pathway molecules in the lung tissue of rats under hyperbaric oxygen exposure / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To study the expression pattern of peroxisome proliferator-activated receptor (PPAR) pathway molecules in rat lung tissue under hyperbaric oxygen exposure.</p><p><b>METHODS</b>Twenty seven male SD rats were randomly divided into hyperbaric normoxia group (0.23 MPa air), hyperbaric oxygen treatment time series group (0.23 MPa oxygen, were exposed for 2 h, 4 h, 6 h or 8 h), continuous small flow of ventilation to maintain cabin O2 concentration > 99%. HE staining of lung tissue morphological changes and application oligo microarray to each time point lung were observed. Part of the PPAR pathway genes were validated by RT-PCR.</p><p><b>RESULTS</b>Compared with hyperbaric normoxia group, the lung injury caused by hyperbaric oxygen treatment gradually deteriorated during the time series. Expression microarray analysis of gene ontology (Go) enrichment analysis results in a class of PPAR pathway class included multiple PPAR pathway molecule. RT-PCR results suggested that PPAR-8 and PPAR-Y were up-regulated in the lung tissue after a long time exposure to hyperbaric oxygen.</p><p><b>CONCLUSION</b>Pro-longed hyperbaric oxygen exposure causing pulmonary oxygen toxicity can induce the activation of the PPAR pathway.</p>

Effect of a simulated He-O2 saturation dive to 65 msw on oxidative stress in humans / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate whether a simulated He-O2 saturation dive to 65 msw would affect oxidative balance in humans.</p><p><b>METHODS</b>Seven divers participated in a simulated saturation dive to 0.75 MPa (65 msw). 24-h urine samples were collected twice before, twice during, and twice after the dive, then were analyzed for contents of superoxide dismutase (SOD), malondialdehyde (MDA), total amino acid (T-AA) and total anti-oxidant capacity (T-AOC). Meanwhile, total urine volume and body weight were measured.</p><p><b>RESULTS</b>The content of T-AA was higher. (P < 0.05) than the base value in final decompression, but reverse to normal at one week after decompression. There were no changes in contents of SOD, MDA and T-AOC during and after the dive compared with their basic value. Total urine volume was lower (P < 0.05, vs basic value) at first day in chamber, then returned to normal. Body weight gradually increased after compression till the end of decompression (higher than basic value, P < 0.05).</p><p><b>CONCLUSION</b>These data indicate that simulated saturation dive to 65 msw may not induce obvious oxidative damage, but it is necessary to monitor 24-h urine volume and oxidative sress by time in order to prevent from tissue injury.</p>

A study of recompression treatment schedule for treating type I decompression illness with medical hyperbaric chamber pressurized / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To 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.</p><p><b>METHODS</b>The recompression treatment schedule D2 was from the decompression treatment tables of <Leaflet for the Treatment of Illness in Compressed Air> 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.</p><p><b>RESULTS</b>In 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).</p><p><b>CONCLUSIONS</b>The 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.</p>