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 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>

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.

Changes of adhesion molecules and adenosine in divers post 480 heliox saturation diving / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the changes of adhesion molecules, cyclic adenosine monophosphate(cAMP) and cyclic guanosine monophosphate (cGMP) in divers post 480 heliox saturation diving.</p><p><b>METHODS</b>Four divers were compressed within 96 hours to depths of 480 m with heliox-oxygen and held at the designated depth for 49 hours, excursion to 493 m during their saturation stay, then decompressed within 302 hours to the surface. The blood samples were collected before compression and post decompression, the expression level of intercellular adhesion molecule-1(ICAM-1), E-selectin, P-selectin, cAMP, cGMP were detected with ELISA analysis box.</p><p><b>RESULTS</b>Compared with the levels of CAMs before compression, the levels of ICAM-1, E-selectin, P-selectin and cGMP in the serum were changed post decompression (P > 0.05). The levels of cAMP were significantly elevated post decompression (629.91 +/- 75.01) nmol/L vs (66.72 +/- 83.15) (P < 0.05).</p><p><b>CONCLUSION</b>The decompression schedule in this heliox saturation diving is safe, the decompression sickness pathology in this diving has not been induced. But the stress response of divers are enhanced by this great depth saturation diving.</p>

Change of coagulation and fibrinolysis in rabbit model with acute decompression sickness and its mechanism / 中国实验血液学杂志

This study was purposed to investigate the changes in coagulation and fibrinolysis pathways in rabbits suffered from the acute decompression sickness(DCS). Model of DCS in rabbits was established. Survival rate and symptoms of DCS in animal model was monitored. The prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen (Fib), fibrinogen degradation product (FDP) and D-dimers were measured before compression and at 0, 3, 24 hours after decompression by latex agglutination semiquantitative methods. The changes of plasmin-antiplasmin complex (PAP), fibrinopeptide A (FPA), plasminogen activator inhibitor 1 (PAI-1) and thrombomodulin (TM) were measured by ELISA at different time points after decompression. The results showed that the model of DCS in rabbits was successfully established. There was a statistically significant extension in APTT, TT, increase of Fib concentration at 15 minutes after decompression, the changes were peaked at 3 hours and recovered at 24 hours after decompression. The concentration of FDP significantly decreased at 3 hours after decompression. The concentration of D-dimers significantly increased at 24 hours after decompression in rabbits model with DCS. FPA concentration was significantly increased at 15 minutes and recovered at 24 hours after decompression. PAP concentration was increased after decompression, but had no significant changes. PAI-1 could not be detected. TM significantly increased after decompression. It is concluded that the acute DCS significantly impacts on blood coagulation system in rabbit model. It is shown that hypocoagulation occurred at initial time and hyperfibrinolysis subsequently, which varied with time. The damage of blood vessel endothelium may be one of the causes of these variations.

The role of marrow derived mesenchymal stem cells in the prevention and treatment of acute graft-versus-host in mice / 中华血液学杂志

<p><b>OBJECTIVE</b>To observe the prevention and treatment of acute graft-versus-host disease (aGVHD) by murine marrow mesenchymal stem cells (MSCs) in vivo.</p><p><b>METHODS</b>Allogeneic aGVHD model was established with lethally irradiated BALB/c recipients receiving allogeneic BM (BMC) and spleen cells (SP) from C57BL/6 with or without mMSCs at different dose and different time posttransplantation. Six groups were set up, group 1 (irradiation control group); group 2 (i.v. BMC only); group 3 (i.v. SP+ BMC); group 4 (i.v. SP + BMC + 1 x 10(5) mMSC at day 0); group 5 (i.v. SP + BMC +5 x 10(5) mMSC at day 0); group 6 (i.v. SP + BMC +1 x 10(5) mMSC at day 7). The survival was monitored daily. mMSCs infected with adenoviral vector (Ad-GFP) were injected into aGVHD model to observe the distribution of MSCs in vivo.</p><p><b>RESULTS</b>(1) Addition of donor mMSCs significantly controlled the lethal GVHD. The survival time (day) in group 1 was 13.5 +/- 2.6, group 3 11.1 +/- 4.0, group 4 26.4 +/- 7.7, group 5 22.7 +/- 9.2, group 6 22.9 +/- 8.2, respectively. The difference between groups 4-6 and group 3 was statistically significant (P < 0.01), but there was no difference among groups 4-6 (P = 0.28); There was less lymphocyte infiltration and architectural disruption in the intestine and spleen of groups 4-6 than that of group 3; (2) mMSCs significantly reduced IFN-gamma and TNF-alpha in the serum of recipient mouse; the levels of IFN-gamma in groups 3, 4, 5, 6 were (607.9 +/- 157.1), (143.6 +/- 37.5), (117.0 +/- 77.8), (131.4 +/- 63.4) ng/L, respectively. And of TNF-alpha were (52.31 +/- 17.95), (6.02 +/- 3.99), (5.21 +/- 0.28), (22.39 +/- 18.21) ng/L, respectively. mMSCs had no effect on allogeneic T cell proliferation in GVHD model but increased apoptosis of allogeneic T cells. The percentage of CD3(+) Annexin V(+)PI(-) in each group were (10.3 +/- 6.6)%, (13.5 +/- 13.8)%, (19.7 +/- 6.0)%, (16.6 +/- 7.3)%, respectively. (3) After intravenous infusion, large numbers of GFP-MSCs lodged in lungs and intestines while small numbers in the liver, spleen and kidney.</p><p><b>CONCLUSIONS</b>MSCs has no effect on proliferation but induce apoptosis of allo-reactive T cells; MSCs can inhibit the second activation of allogeneic T cells, significantly reduce the secretion of IFN-gamma and TNF-alpha; MSCs might be able to repair GVHD target tissues by extensive distribution to lungs, intestines, and liver of the animals.</p>

Blocking ICOS-B7h signal pathway by ICOS-Ig fusion protein inhibits function of allogeneic T lymphocytes / 中国实验血液学杂志

Inducible costimulatory molecule (ICOS), a CD28 family member expressed on activated T cells, plays an important roles in T cell activation and effector function. This study was purposed to investigate the effect of blocking ICOS-B7h signal pathway by ICOS-Ig fusion protein on allogeneic reactive T cells and its mechanism. CHO cells stably and highly expressing ICOS-Ig were established, while the human ICOS-Ig fusion protein was harvested and purified from supernatant of CHO cells transfected with pSecTag2/Hygro A-ICOS-Ig. The CD4(+) cells from spleen of C57BL/6 mice were used as reactive cells, the bone marrow derived dendritic cells (DCs) from BALB/C mice were used as stimulatory cells, these cells were treated with different concentrations of ICOS-Ig or human Ig (h-Ig) as control. The results showed that the target protein with molecular weigh 54 kD and endotoxin level < 10 EU/ml was gained. The ICOS-Ig (> or = 10 microg/ml) could significantly inhibited the proliferative effect of allogeneic reactive T cells resulting from stimulation of DCs (p < 0.01). ICOS-Ig did not influence the activation of CD4(+) T cells. ICOS-Ig concentration positively related to the apoptosis of CD4(+) T cells. The percentages of CD4(+) Annexin V(+)PI(-) cells in simple stimulated group, ICOS-Ig 10 microg/ml group and ICOS-Ig 20 microg/ml group were 15.1%, 26.4% and 33.6% respectively. ICOS-Ig decreased secretion of TNFalpha and increased secretion of IL-4. It is concluded that the ICOS-Ig fusion protein has bioactivity of inhibiting T cell proliferation and altering the polarization of T helper cells to Th2 cells which promotes the apoptosis of allogeneic reactive T cells but had no effect on the activation of allo-reactive CD4(+) T cells.