(8.11)--一氧化氮调控力竭运动诱导的红细胞变形能力下降的研究进展.pdfVIP

(8.11)--一氧化氮调控力竭运动诱导的红细胞变形能力下降的研究进展.pdf

一氧化氮调控力竭运动诱导的红细胞变形能力

下降的研究进展

摘要红细胞(redbloodcell,RBC)的变形能力对于保障其氧运输功能的正常发挥具有重要

作用。力竭运动导致机体缺氧,出现氧化应激反应,机体氧化还原失稳态,RBC膜结构被破坏。血

红蛋白(hemoglobin,Hb)也将被氧化成高铁血红蛋白(methemoglobin,MetHb),与RBC膜骨架蛋白

交联并最终引起RBC变形能力下降。一氧化氮(nitricoxide,NO)不仅能够作为内皮舒张因子参与

调节机体血流稳态,近年来还发现NO具有调控RBC变形能力的功能。该文以NO调控RBC膜的氧

化损伤反应为切入点,梳理NO调控力竭运动诱导的RBC变形能力下降的作用机制,旨在为促进力

竭运动后机体氧运输功能的恢复提供理论依据。

关键词一氧化氮;红细胞变形能力;氧化还原失稳态;力竭运动

ResearchProgressofNitricOxideinRegulatingtheDecline

ofErythrocyteDeformabilityInducedbyExhaustiveExercise

QIQinke,WANGDan,LIZongxiang,LIUYanzhong,LANLinfei,LIUYiping*

(ProvincialUniversityKeyLaboratoryofSportandHealthScience,DepartmentofPhysicalEducationandSportSciences,

FujianNormalUniversity,Fuzhou350007,China)

AbstractThedeformabilityofRBC(redbloodcell)playsanimportantroleinensuringthenormalfunc-

tionofoxygentransport.Exhaustiveexerciseleadstohypoxia,oxidativestressreaction,oxidation-reductionin-

stabilityanddestructionoferythrocytemembranestructure.Hemoglobinwillalsobeoxidizedtomethemoglobin,

whichwillbecross-linkedwitherythrocytemembraneskeletonproteinandeventuallyleadtothedeclineoferyth-

rocytedeformability.Nitricoxidecannotonlyparticipateintheregulationofbloodflowhomeostasisasanendo-

thelialrelaxingfactor,butalsohasbeenfoundtohavethefunctionofregulatingerythrocytedeformabilityinrecent

years.Thisarticletakestheregulationofnitricoxideontheoxidativedamagereactionoferythrocytemembraneas

thestartingpoint,andcombsthemechanismofnitricoxideregulatingthedeclineoferythrocytedeformabilityin-