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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Limb remote ischemia per-conditioning protects the heart against ischemia–reperfusion injury through the opioid system in rats
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Limb remote ischemia per-conditioning protects the heart against ischemia–reperfusion injury through the opioid system in rats

机译：肢体远程缺血每调保护心脏通过大鼠阿片类药物系统免受缺血再灌注损伤

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Remote ischemia per-conditioning (RPerC) has been demonstrated to have cardiac protection, but the underlying mechanism remains unclear. This study aimed to investigate the mechanism underlying cardiac protection of RPerC. Adult male Sprague–Dawley rats were used in this study. Cardiac ischemia/reperfusion (I/R) was induced by 30 min of occlusion and 3 h of reperfusion of the left anterior descending coronary artery. RPerC were performed by 5 min of occlusion of the right femoral artery followed by 5 min of reperfusion for three times during cardiac ischemia. The hemodynamics, left ventricular function, arrhythmia, and infarct area were measured. Protein expression levels of endothelial nitric oxide synthase (eNOS), inducible NOS (iNOS), protein kinase C-ε (PKC_(ε)), and PKC_(δ) in the myocardium were assayed. During I/R, systolic artery pressure and left ventricular function were decreased, infarct area was increased, and arrhythmia score was increased ( P P < 0.05). The cardiac protective effects of RPerC were prevented by naloxone or glibenclamide. Also, RPerC increased the protein expression levels of eNOS, iNOS, PKC_(ε), and PKC_(δ) in the myocardium compared with control rats. These effects were blocked by naloxone, an opioid receptor antagonist, and glibenclamide, an ATP-sensitive K~(+) channel blocker (K_(ATP)). In summary, this study suggests that RPerC protects the heart against I/R injury through activation of opioid receptors and the NO–PKC–K_(ATP) channel signaling pathways.
机译：已经证明了遥控缺血（RPERC）具有心脏保护，但潜在的机制仍然不清楚。本研究旨在调查RPERC的心脏保护潜在机制。在这项研究中使用了成年男性Sprague-Dawley大鼠。通过30分钟的闭塞诱导心脏缺血/再灌注（I / R）和左前期下降冠状动脉的再灌注3小时。 RPERC在右股动脉的5分钟内进行，然后在心脏缺血期间进行了5分钟的再灌注三次。测量血流动力学，左心室功能，心律失常和梗塞区域。测定内皮一氧化氮合酶（eNOS），诱导型NOS（InOS），蛋白激酶C-ε（PKC_（ε））和心肌中的PKC_（δ）的蛋白质表达水平。在I / R期间，减少收缩动脉压和左心室功能，梗死区域增加，增加了心律失常（P <0.05）。通过纳洛酮或Glibenclamide预防Rperc的心脏保护作用。此外，与对照大鼠相比，RPERC增加了心肌中的烯烯，InOS，PKC_（ε）和PKC_（δ）的蛋白质表达水平。这些效果被纳洛酮，阿片类受体拮抗剂和Glibenclamide，ATP敏感K〜（+）通道阻断剂（K_（ATP））阻断。总之，该研究表明，RPERC通过激活阿片受体和NO-PKC-K_（ATP）信道信号传导途径来保护心脏免受I / R损伤。

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