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简介：Objective:Tostudytheclinicaltherapeuticeffectofanisodamineonrespiratoryfunctionafterseverebraininjury.Methods:Ninetypatientswithrespiratorydysfunctionfollowingseverebraininjuryweredividedintotwogroups:atreatmentgroup(n=45,treatedwithroutinetherapyplusanisodamine)andacontrolgroup(n=45,treatedwithroutinetherapyonly).Thepulmonaryventilationfunctionandoxygenationfunctionwerecomparedbetweenthetwogroups.Results:Inthetreatmentgroup,12hoursaftertreatmenttherespiratoryratereduced,thepartialpressureofcarbondioxide(PCO2),thepartialpressureofoxygeninarterialblood(PaO2)andoxygenationexponentincreased,thedeadspaceventilationdoseandthepulmonaryalveolus-partialpressureofarterialoxygendifferencedecreased,andtheventilationfunctionoftherespiratorytractandpulmonaryoxygenationfunctionimproved.Therewasasignificantdifferencebetweenthetwogroups(P<0.01).Noside-effectwasfoundexceptaslightincreaseofintracranialpressureandheartrate.Conclusions:Anisodaminecanimprovepulmonaryventilationfunctionandoxygenationfunctionanddecreasetheincidenceofhypoxemiamarkedly.Itiseffectiveintreatingrespiratorydysfunctionafterseverebraininjury.

简介：Objective:Tostudytheeffectsofmagnesiumsulfateonbrainmitochondrialrespiratoryfunctioninratsafterexperimentaltraumaticbraininjuryandthepossiblemechanism.Methods:ThemiddledegreebraininjuryinratswasmadebyBIM-IIImulti-functionimpactingmachine.Thebrainmitochondrialrespiratoryfunctionwasmeasuredwithoxygenelectrodeandtheultra-structuralchangeswereobservedwithtransmissionelectronmicroscope(TEM).Results:1.ThebrainmitochondrialrespiratorystageIIIandrespirationcontrolratereducedsignificantlyintheuntreatedgroupswithin24and72hours.ButtreatedGroupAshowedcertaindegreeofrecoveryofrespiratoryfunction;treatedGroupBshowedfurtherimprovement.2.UntreatedGroup,treatedGroupsAandBhaddifferentdegreesofmitochondrialultra-structuraldamagerespectively,whichcouldbeattenuatedafterthetreatmentwithmagnesiumsulfate.Conclusions:Themitochondrialrespiratoryfunctiondecreasessignificantlyaftertraumaticbraininjury.ButitcanbeapparentlyimprovedaftermagnesiumsulfatemanagementalongwiththeattenuateddamageofmitochondriadiscoveredbyTEM.Thelongercourseoftreatmentcanobtainabetterimprovementofmitochondrialrespiratoryfunction.

简介：探索二的保护的效果的目的与后部的手足的压碎损害在肠的mucosa障碍上ischemicpostconditioning(IP)录入兔子。这研究在损伤外科的部门在8月和2008年12月之间被进行的方法，弹跳的医院，第三所军事医药大学，重庆，中国。对兔子的后部的手足的压碎损害的模型被25kg目标第一开发，恰好后部的手足由木藤条修理了，然后IP的二种类型包括堵塞/打开被建立普通肠骨的动脉和静脉或者(传统的IP，IPA)并且binding/loosening受伤后部的手足的proximum或者(修改IP，IPB)。36只雄的新西兰白兔子随机被划分成三个组：IPA组，IPB组和控制组织，带着在每个组的12只兔子。肼oxidase(DAO)和肠的丰满的酸绑定的蛋白质(I-FABP)的浆液层次在损害以后在2，6，12和24个小时被检测。回肠的病理学的变化在损害以后在24个小时被检验。浆液在IPA和IPB组在损害以后在2，6，12和24个小时I-FABP铺平的结果有重要减少，与控制组相比。DAO层次也在损害以后在2和6个小时显示出一样的变化趋势，但是没显示出二个IP组之间的重要差别。在回肠的病理学的变化的差别都没在三个组之中被发现。结论IP能在兔子在后部的手足压碎损害的模型上保护肠的mucosa障碍功能。同时，修改IPB显示出象传统的IPA的一样的保护，并且值得在诊所适用。

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