The Changes Of Histopatholoyg Of ThpeⅡ Decompression Sickness In Rabbits And The Preliminary Study Of Pathogenesis

ObjectiveIn this study, we have attempted to establish the model of Type Ⅱ DecompressionSickness in rabbits, to observe the pathological changes with light and transmissionelectron microscopy, to detect the expression level of GFAP in spinal cord throughinmmunohistochemistry, and to detect the expression level of DCS-related genes andproteins using whole genome oligo microarrays methods. And our study was topreliminarily explore the pathogenesis of TypeⅡ DCS and the effect of HBO.Methods1. We established the model of Type ⅡDecompression Sickness in rabbit and devidedthe rabbits into different groups.2. We observed the manifestations of all groups after the rabbits out of the cabin, thenhad an anatomy of them and collected samples of all kinds of tissues, which would to beexamined by light microscopy. Spinal cord of the rabbits was removed and examined bylight microscope, electromicroscope examination, immunohistochemistry.3. The spinal cord of groups of DCS and controls were detected by using the wholeGenome Oligo Microarrays.Results1. We established the model of Type ⅡDecompression Sickness in rabbit. Thepressure was increased to800Kpa with5min using compressed air, maintain at800Kpafor60min, and then was decompressed to normal pressure within3~5min.2. The rabbits in the group of DCS had typical TypeⅡ DCS symptoms, such as hindlimbs motion obstacle, dyspnea and so on. The other three groups had no obviously clinicalsymptoms. There were lots of histological abnormalities to be seen with light microscopyin the group of DCS，such as, focal pulmonary atelectasis and hemorrhages could be seenwith many dilated vessels, the other tissues had different degrees of pathological changes. There were lots of histological abnormalities in the spinal cord to be seen with lightmicroscopy in the group of DCS. There were a lot of numerous, non-staining,space-occupying lesions in the white matter of the cords, axon edema and arrangingdisorderly. Transmission electron microscopic examination demonstrated that the whitematters’ architecture had been disrupted and the axon demyelinated. Immunohistochemicalresults: We found that DCS could induce the expression of GFAP in spinal cords. Theexpression of GFAP became more and more positive from group of control, safetydecompression/Hyperbaric Oxygen treatment to group of DCS.3. The whole Genome Oligo Microarrays showed a lot of differentially expressedgenes, which related to inflammation, cell cycles, hormone, transcription factors and so on.TNF-, parathyroid hormone, inhibitor of CDK were up-regulated genes, while IL-12A,CAP18，MRP8, acyl-CoA synthetase short-chain family member2were down-regulatedgenes.Conclusion1. We successfully established the model of Type ⅡDecompression Sickness inrabbit.2. Through light microscope, it was demonstrated that spinal cords and lungs are thetwo mostly injured organs of TypeⅡ Decompression Sickness in rabbits, accompanied withthe seriously pathologic changes of the whole body.3. We inferred that there were two direct pathogenesis of Type ⅡDecompression, onewas gas bubbles in the capillaries, and the other was “autonomous bubbles”. Tissue edema,never fiber demyelination and gliogyte hyperplasia were observed in spinal cord ofType ⅡDecompression Sickness in rabbits.The therapy of HBO is very important forTypeⅡ D ecompression Sickness.4. The whole Genome Oligo Microarrays showed a lot of differentially expressedgenes, which related to inflammation, cell cycles, hormone, transcription factors and so on.