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ATP敏感性钾通道对腺苷受体诱导的心脏预处理延迟效应的影响

The Influence of ATP-sensitive K^+ Channels on Delayed Preconditioning with Adenosine A_1 Receptor Analogue in Rat Hearts
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摘要 目的研究以腺苷A1 受体激动剂预处理的延迟保护效应与心肌三磷酸腺苷(ATP)敏感性钾通道的关系。方法Wistar大鼠随机分4组,其中PS、PG组以CCPA预处理 ,IC组仅注射CCPA溶剂 ,GC组不作CCPA预处理。24h后取出心脏 ,以改良Langendorff灌注装置制成离体心脏模型。缺血前30minPG、GC组先经主动脉灌注优降糖。平衡灌注后4℃改良St.Thomas心麻液诱导心脏停搏 ,维持12~15℃缺血180min.。之后复灌37℃氧合平衡液60min。观察心功能、ATP等指标。结果在复灌60min时左室压力上升和下降最大速率恢复率 (±dp/dtmax,% )及心肌ATP含量均高于PG、GC、IC三组 ,差异都具有显著性 (P<0.01);PG、GC、IC组间无显著性差异(P>0.05)。结论以腺苷A1 Objective To study the influence of ATP-sensitive K + channels on the delayed preconditionig with adenosine A1receptor analogue.Methods Male Wistar rats in groups PS,PG were preconditioned with adenosine A1receptor analogue2-chloro-N6-cyclopen-tyladenosine(CCPA),while solvent of CCPA was givˉen in IC.24hours later,the rat hearts were isolated and perfused with H-K buffer solution on the Langendorff apˉparatus.ATP-sensitive K + channels blocker,glibenclamide was given in the PG and GC groups30minutes before ischemia,and isolated hearts in all groups were subjected to180minutes hypothermic ischemia with intermittent perfusion of modified St.Thomas solution,and reperfused with37℃H-K buffer for60minutes.Results The left ventricular systolic function recovery rates(±dp/dt max ,%)in groups PS,PG,GC,IC were72.62±16.28,49.95±12.77,45.92±9.06,51.38±13.87,while the left ventricular diastolic function recovery rates(-dp/dt max ,%)were68.16±19.22,48.79±21.98,50.56±16.53,49.60±12.21,and myocardial ATP level(10 -3 μmol/g.wet)were5.12±0.87,1.48±0.71,1.69±0.64,1.27±0.33,respectively.These in PS group were much better or higher than those in PG,GC,IC,where differences were significant(P<0.01),but differˉences among PG,GC,IC were not significant.Conclusions Adenosine A1receptor analogue may induce late phase of preconditioning and opening of ATP-sensitive K+channels plays an essential role in the late phase of preconditioning.
出处 《中国微循环》 2004年第4期216-218,共3页 Journal of Chinese Microcirculation
关键词 腺苷 预处理 ATP敏感性钾通道 Adenosine Preconditioning ATP-sensitive K + channels
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