ATP-sensitive K+ channels mediate the delayed cardioprotective effect of adenosine A1 receptor activation
ATP-sensitive K+ channels mediate the delayed cardioprotective effect of adenosine A1 receptor activation
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DOI：
10.1006/jmcc.1999.0927
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发表时间：
1999-05-01
影响因子：
5
通讯作者：
Yellon, DM
中科院分区：
文献类型：
--
作者：
Baxter, GF;Yellon, DM
腺苷A受体刺激可在数小时后增加心肌对缺血的恢复力，但其保护机制尚不清楚。我们假设A受体诱导的延迟心脏保护是由Ii通道打开介导的。兔分别以生理盐水或选择性A受体激动剂3-氯- n -6-环戊基腺苷（CCPA） 0.1 mg/kg滴注预处理，24h后麻醉，左冠状动脉闭塞（CAO） 30min，再灌注120min。术前20分钟，静脉注射格列苯脲0.3 mg/kg、5-羟癸酸钠（5- hd） 5 mg/kg或相应体积的载药溶液。采用三苯四唑法评估梗死面积占缺血危险体积的百分比（I/R%）。在没有格列本脲或5-HD的情况下，CCPA预处理导致梗死的显著限制(I/R 23.4 +/- 3.3% vs盐水预处理动物的39.6+/-2.6%，P
Adenosine A, receptor stimulation increases myocardial resilence to ischaemia many hours later but the mechanism of protection is unclear. We hypothesized that A, receptor-induced delayed cardioprotection is mediated by Ii, channel opening. Rabbits were pretreated with saline or the selective A, receptor agonist 3-chloro-N-6-cyclopentyladenosine (CCPA), 0.1 mg/kg i.v. After 24h, they were anaesthetized and subjected to 30 min left coronary artery occlusion (CAO) and 120 min reperfusion. Twenty minutes before CAO, either glibenclamide 0.3 mg/kg, sodium 5-hydroxydecanoate (5-HD) 5 mg/kg, or a corresponding volume of vehicle solution were given i.v. Infarct size as a percentage of ischaemic risk volume (I/R%) was assessed by triphenyltetrazolium. In the absence of either glibenclamide or 5-HD, CCPA pretreatment resulted in significant limitation of infarction (I/R 23.4 +/- 3.3% vs 39.6+/-2.6% in saline pretreated animals, P