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ID:25169628
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时间:2018-11-17
《mitokatp通道开放对离体兔心缺血再灌注损伤的保护作用论文》由会员上传分享,免费在线阅读,更多相关内容在工程资料-天天文库。
1、mitoKATP通道开放对离体兔心缺血再灌注损伤的保护作用论文.freelas停搏液(K+16mmol/L)至心脏停跳,45min后再灌注20min,药物于心脏停跳前灌注15min。对比观察Pinacidil、Diazoxide及其与5-HD合用时心脏的功能指标、冠脉血流量以及再灌注末心肌组织中腺苷酸含量、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性和心肌酶的变化。结果P组、D组、HP组再灌注后复跳时间、心功能的恢复率、心肌能量保存、SOD活性均显著高于C组,心肌酶、MDA的含量显著低于C组,HP组心功能的恢
2、复、能量保存差于P组,心肌酶、MDA的含量高于P组。结论肌纤维膜型(sarcKATP通道)和线粒体型(mitoKATP通道)KATP通道共同参与对心肌缺血再灌注损伤的保护作用.freelitoKATP通道起主导作用。【关键词】mitoKATP通道;缺血再灌注损伤;离体家兔;心脏【Abstract】ObjectiveToinvestigatetheprotectiveeffectsofdifferentATP-sensitivepotassium(KATP)channelopens,PinacidilandDiazo
3、xide,onmyocardiuminjuryinisolatedrabbitheartscausedbyischemia/reperfusionandpossiblechangesafterapplicationofATP-sensitivepotassiumchannelblocker,5-HD.MethodsObservationadeonrabbitheartsperfusedlydividedintofourselectedgroups:1.Pinacidil;2.Diazoxide;3.5-HD+Pin
4、acidil;4.5-HD+Diazoxide.Allgroupsinutesocclusion,thenfolloinutesreperfusionascardiacstoppedfunctioningbycoldcardioplegia.AnyoneofPinacidil,Diazoxide,PinacidilorDiazoxidemixedinutesbeforecardioplegicheartrestedinexperimentalgroup.Hemodynamicsvariables,levelsofa
5、deninenucleotidesandlipidperoxideofthemyocardiumeasured.Results(1)InGroupP,GroupDandGroupHP,therecoveryofmyocardialcontractilityandheartrateyocardiumandhadmuchloyocardialadenosinetriphosphate(ATP)(P<0.05or0.01)uchhigher.(2)InGroupHP,hoyocardialcontractilityand
6、heartratecouldnotbeasgoodasGroupP,MDAlevelofmyocardiumandreleaseamountofalbumenchannelopenesmayenhancemyocardialprotectionagainstischmia/reperfusioninjury.Theaboveeffectofmyocardialprotectionchannelblocker:5-HD.Theseresultsshoacologicalagentsimplicatemitochond
7、riaandsarcolemmalKATPchannelsarenotimportantinischemiccardioprotection.【KeyitochondrialATPsensitivepotassiumchannel;ischemia/reperfusioninjury;isolatedrabbit;hearts1983年,Noma[1]应用膜片钳技术首先在豚鼠心肌细胞上发现ATP敏感性钾通道(KATP通道)。随着对KATP通道深入的研究发现KATP通道是将细胞代谢和细胞电活动耦联起来,从而调节细胞功
8、能(如胰岛β2细胞的分泌功能、血管舒缩功能、缺血预适应中对心肌的保护作用等)的重要通道。本实验室的前期试验表明ATP敏感性钾通道开放剂(KCOs)Pinacidil对离体兔心及外循环心内直视手术下的犬心缺血再灌注损伤具有保护作用,KATP通道的激活可能参与心脏内源性保护机制[2,3]。随着分子生物学技术的发展发现心肌细胞有sarcKATP通道和mitoKAT
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