NovelAcuteRetinalArteryIschemiaandReperfusionModelinNonhumanPrimatesStrokeresearch-articleEarlyRecent,July20,./STROKEAHA..本文由“天纳”临床学术信息人工智能系统自动翻译点击文末“阅读原文”下载本文PDFBackgroundandPurpose:Theretina,asanexternallylocatedneuraltissue,offersuniqueadvantagesininvestigatingtheeffectoftherapeuticinterventiononthebrain.Inthisstudy,weputforthaclinicallyrelevantmodelofretinalischemiaandreperfusioninnonhumanprimates.视网膜作为一种位于外部的神经组织，在研究治疗性干预对大脑的影响方面具有独特的优势。在这项研究中，我们提出了一个与临床相关的非人灵长类视网膜缺血再灌注模型。Methods:Acuteretinalarteryischemiaandreperfusionwasinducedbyinjectinganautologousclotintotheophthalmicarteryofadultrhesusmonkeys,andrecanalizationwasachievedbyfocalthrombolysiswithtPA(tissue-typeplasminogenactivator).Digitalsubtractionangiographyandfluoresceinangiographywereusedtoevaluatebloodflowintheretinaandthechoroid.Electroretinogram,opticalcoherencetomography,andhematoxylinandeosinstainingwereusedtoevaluatethestructureandfunctionoftheretinaafterischemia.将自体血块注入成年恒河猴眼动脉，诱导视网膜动脉急性缺血再灌注，用组织型纤溶酶原激活剂（tPA）局部溶栓后再通。数字减影血管造影和荧光素血管造影用于评估视网膜和脉络膜的血流。用视网膜电图、光学相干断层扫描、苏木精伊红染色评价缺血后视网膜的结构和功能。Results:Digitalsubtractionangiographyandfluoresceinangiographyimagesconfirmedocclusionoftheophthalmicandcentralretinalarteries,aswellasrecanalizationaftertPAthrombolysis.Electroretinogramindicatedretinalfunctionaldamagefollowingischemia,andthrombolysispartiallyrescueditsimpairment.Opticalcoherencetomographyandhematoxylinandeosinstainingrevealedischemia-inducedchangesintheretina,andtPApartiallymitigatedthesedamages.数字减影血管造影和荧光素血管造影图像证实眼动脉和视网膜中央动脉阻塞，以及tPA溶栓后的再通。视网膜电图显示缺血后视网膜功能损害，溶栓治疗部分恢复了其损害。光学相干断层扫描和苏木精伊红染色显示缺血引起的视网膜改变，tPA部分减轻了这些损伤。Conclusions:Thisnovelacuteretinalarteryischemiaandreperfusionmodelinrhesusmonkeysmaycloselysimulateretinalischemia/reperfusioninclinicalpracticeandprovideanoptimalplatformforscreeningneuroprotectivestrategies.这种新的恒河猴急性视网膜动脉缺血再灌注模型可以在临床上模拟视网膜缺血/再灌注，为筛选神经保护策略提供了一个最佳的平台。FootnotesThismanuscriptwassenttoEngH.Lo,ConsultingEditor,forreviewbyexpertreferees,editorialdecision,andfinaldisposition.*DrGao,Wu,andLiucontributeequally.ForSourcesofFundingandDisclosures,seepage.TheDataSupplementisavailablewiththisarticleat
