首页> 外文期刊>American Journal of Physiology >Stretch-induced protection shares a common mechanism with ischemic preconditioning in rabbit heart.
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Stretch-induced protection shares a common mechanism with ischemic preconditioning in rabbit heart.

机译:拉伸诱导的保护与兔心脏缺血预处理具有共同的机制。

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摘要

We sought to determine whether stretch-induced preconditioning may be related to activation of adenosine receptors, ATP-sensitive K+ (K+ATP) channels, and/or protein kinase C (PKC) in the rabbit heart. Anesthetized rabbits underwent 30 min of coronary artery occlusion followed by 3 h of reperfusion. Ischemic preconditioning was induced by one episode of 5 min of ischemia followed by 5 min of reperfusion, and stretch preconditioning was induced by a transient volume overload. The abilities of gadolinium (Gd3+), a blocker of stretch-activated channels, glibenclamide (Glib), a blocker of K+ATP channels, 8-(p-sulfophenyl)-theophylline (8-SPT), a blocker of adenosine receptors, and polymyxin B (PMXB), an antagonist of PKC, to prevent the infarct size-limiting effect of stretch-induced preconditioning were evaluated. Because the infarct size-reducing effect of stretch occurred in the absence of ischemia and was prevented by previous administration of Gd3+, Glib, 8-SPT, and PMXB, we propose that activation of mechanosensitive ion channels protects the rabbit heart from subsequent sustained ischemic insult, likely through a mechanism that involves downstream activation of PKC, adenosine receptors, and/or K+ATP channels.
机译:我们试图确定拉伸诱导的预处理是否可能与兔心脏中腺苷受体,ATP敏感的K +(K + ATP)通道和/或蛋白激酶C(PKC)的激活有关。麻醉的兔子进行30分钟的冠状动脉闭塞,然后再灌注3小时。缺血预适应是由5分钟的缺血发作后再灌注5分钟引起的,而拉伸预适应则由短暂的体积超负荷诱导。 stretch(Gd3 +),舒张激活通道的阻滞剂,格列本脲(Glib),K + ATP通道的阻滞剂,8-(对-磺基苯基)-茶碱(8-SPT),腺苷受体的阻滞剂的功能,评估了PKC的拮抗剂多粘菌素B(PMXB)预防拉伸诱导的预处理的梗塞大小限制作用。因为拉伸的梗死面积缩小效应是在不存在缺血的情况下发生的,并且可以通过先前施用Gd3 +,Glib,8-SPT和PMXB来预防,所以我们建议激活机械敏感离子通道可保护兔心脏免于随后的持续缺血性损伤,可能是通过涉及PKC,腺苷受体和/或K + ATP通道下游激活的机制引起的。

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