减压病时血小板的功能变化及机制研究-潜水医学专业论文 word格式.docx

炎性介质，可能在减压病引起的脂代谢紊乱中起重要作用。另外，反复减压不当产生的显性和/或隐性气泡造成血小板计数进行性下降，血液持续高粘状态，使骨缺血坏死效应累积，最终形成减压性骨坏死。因此，需要长期、规范的高压氧治疗，才能得到较满意的疗效。关键词：减压病；血小板；肺；流式细胞术；代谢组学；核磁共振；减压性骨坏死AbstractDecompressionsicknes（sDCS）,pressurerelatedinjury,isthatillnesswhichfollowsareductioninenvironmentalpressuresufficienttocausetheformationofbubblesfromgasesdissolvedinbodytissues.DCScanbedividedintotwotypes:TypeIDCS(mild)ischaracterizedbypain,pruritus,skinmarblingandlymphaticinvolvement;whileTypeIIDCS(severe)includesallpatientswhohavepulmonarysymptoms,hypovolemicshockorthemoreserioussymptomsorsignsofnervoussysteminvolvement.Acuteseveredecompressionsicknesshashighmortalityintheworldwidebecauseoffeweffectivetreatment.Unsafehyperbaricexposureisknowntoaffectthesystemhaemorheologyofanimal,impairingthecapillarybloodvesselandtissuearound,andcausinginflammatorychangeslikehemorrhageandexudation.Atthattime,plateletaggregationwasobservedinthelung.Platelets,activeparticles,areknowntorelatewithavarietyofpathologicalprocessesanddiseasesnow.Inadditiontoprocoagulantrole,theplateletisalsoinvolvedinthrombosisandinflammationbythewaysofadhesionandinteractionwithotherinflammatorycellsthroughmanyproinflammatoryfactorstheysecreted.Previousresearcheshaveinvestigatedthechangesofplateletcountandmembraneglycoproteinsindifferentdivingmodes,includingunsafedecompression.Butthereisnomechanismreported.Inpresentstudy,wewoulddiscusstheroleofplateletsinthepathogenesisofacutedecompressionsicknesswithpulmonaryinjuryfromtwoaspects:inflammatorysignalingandmetabolicregulatorynetworks.Methods:Inthisstudy,wefirstseletedNewZealandrabbitsandSDratsastheexperimentalmodelofacuteDCSbyunsaferapiddecompression(RD)from0.7MPa.Plateletcountweredetectedat15min,1h,3h,24hafterdecompression,togetherwithmembraneglycoproteinsexpressiondetectedbyflowcytometrywithFITClinkedpolyclonalantibody.Thelunginjurywereobservedbypathologicalstaining,andtheexpressionofMac-1,IL-8,MCP-1,andMMP-9inthelungtissueweredetectedwiththeimmunohistochemical(IHC)method.TheconcentrationsofTXA2