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首页> 外文期刊>American Journal of Physiology >Sites of action of adenosine in interorgan preconditioning of the heart.
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Sites of action of adenosine in interorgan preconditioning of the heart.

机译：腺苷在心脏器官间预处理中的作用部位。

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The mechanism underlying interorgan preconditioning of the heart remains elusive, although a role for adenosine and activation of a neurogenic pathway has been postulated. We tested in rats the hypothesis that adenosine released by the remote ischemic organ stimulates local afferent nerves, which leads to activation of myocardial adenosine receptors. Preconditioning with a 15-min mesenteric artery occlusion (MAO15) reduced infarct size produced by a 60-min coronary artery occlusion (60-min CAO) from 68 +/- 2% to 48 +/- 4% (P < 0.05). Pretreatment with the ganglion blocker hexamethonium or 8-(p-sulfophenyl)theophylline (8-SPT) abolished the protection by MAO15. Intramesenteric artery (but not intraportal vein) infusion of adenosine (10 microg/min) was as cardioprotective as MAO15, which was also abolished by hexamethonium. Whereas administration of hexamethonium at 5 min of reperfusion following MAO15 had no effect, 8-SPT at 5 min of reperfusion abolished the protection. Permanent reocclusion of the mesenteric artery before the 60-min CAO enhanced the cardioprotection by MAO15 (30 +/- 5%), but all protection was abolished when 8-SPT was administered after reocclusion of the mesenteric artery. Together, these findings demonstrate the involvement of myocardial adenosine receptors. We therefore conclude that locally released adenosine during small intestinal ischemia stimulates afferent nerves in the mesenteric bed during early reperfusion, initiating a neurogenic pathway that leads to activation of myocardial adenosine receptors.
机译：尽管已经假定了腺苷和神经源性通路的激活作用，但心脏器官间预调节的基本机制仍然难以捉摸。我们在大鼠中测试了由远端缺血器官释放的腺苷刺激局部传入神经，从而激活心肌腺苷受体的假说。用15分钟的肠系膜动脉闭塞（MAO15）进行的预处理将60分钟的冠状动脉闭塞（60分钟CAO）产生的梗塞面积从68 +/- 2％降低到48 +/- 4％（P <0.05）。用神经节阻滞剂六甲铵或8-（对-磺基苯基）茶碱（8-SPT）进行的预处理取消了MAO15的保护作用。肠系膜内动脉（但非门静脉）输注腺苷（10微克/分钟）与MAO15一样具有心脏保护作用，六甲铵也取消了该作用。在MAO15后再灌注5分钟时给予六甲铵没有效果，而在再灌注5分钟时使用8-SPT取消了保护。在60分钟的CAO之前永久性肠系膜动脉的再闭塞可增强MAO15的心脏保护作用（30 +/- 5％），但在肠系膜动脉再闭塞后给予8-SPT时，所有保护作用都将被取消。总之，这些发现证明了心肌腺苷受体的参与。因此，我们得出的结论是，在小肠缺血期间局部释放的腺苷会在早期再灌注过程中刺激肠系膜床的传入神经，从而引发导致心肌腺苷受体活化的神经源性途径。

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