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首页> 外文期刊>American Journal of Physiology >Humoral transfer and intramyocardial signal transduction of protection by remote ischemic perconditioning in pigs, rats, and mice
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Humoral transfer and intramyocardial signal transduction of protection by remote ischemic perconditioning in pigs, rats, and mice

机译：猪，大鼠和小鼠远程缺血性能的体液转移和肌动脉内信号转导

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Remote ischemic perconditioning (RPER) during ongoing myocardial ischemia reduces infarct size. The signal transduction of RPER's cardioprotection is still largely unknown. Anesthetized pigs were therefore subjected to RPER by 4?×?5 min/5 min of hindlimb ischemia-reperfusion during 60 min of coronary occlusion before 3 h of reperfusion. Pigs without RPER served as placebo (PLA). The phosphorylation of Akt and ERK [reperfusion injury salvage kinase (RISK) pathway] and STAT3 [survivor activating factor enhancement (SAFE) pathway] in the area at risk was determined by Western blot analysis. Wortmannin/U0126 or AG490 was used for pharmacological RISK or SAFE blockade, respectively. Pig plasma/plasma dialysate sampled after RPER or PLA, respectively, was transferred to isolated rat and mouse hearts subjected to 30 min/120 min of global ischemia-reperfusion. Mitochondria were isolated from rat hearts at early reperfusion. Isolated mouse cardiomyocytes were subjected to 1 h of hypoxia/5 min of reoxygenation without and with prior plasma dialysate incubation. RPER reduced infarct size in pigs to 21 ±?15% versus 44 ±?9% in PLA (percentage of the area at risk, mean?±?SD, P < 0.05) and increased STAT3 phosphorylation at early reperfusion. AG490 but not RISK blockade abolished the protection. RPER plasma/plasma dialysate reduced infarct size in rat (22 ±?3% of ventricular mass vs. 40 ±?11% with PLA plasma, P < 0.05) and mouse (29 ±?4% vs. 63 ±?8% with PLA plasma dialysate, P < 0.05) hearts and improved mitochondrial function (e.g., increased respiration, ATP formation, and calcium retention capacity and decreased reactive oxygen species formation). RPER dialysate also improved the viability of mouse cardiomyocytes after hypoxia/reoxygenation. RISK or SAFE blockade each abrogated these beneficial effects.NEW & NOTEWORTHY Remote ischemic perconditioning salvages the myocardium in patients with acute infarction. We identified a signal transduction with humoral transfer and STAT3 activation in pigs and an involvement of reperfusion injury salvage kinases and STAT3 in rat and mouse hearts, along with better cardiomyocyte viability and mitochondrial function.
机译：在持续的心肌缺血期间远程缺血性缺血（RPR）减少了梗塞大小。 RPER的心脏保护的信号转导仍然很大程度上是未知的。因此，在再灌注3小时之前，在4次冠状动脉闭塞期间，将麻醉的猪进行4〜×5分钟的后肢缺血再灌注。没有朗顿的猪用作安慰剂（PLA）。 AKT和ERK的磷酸化[再灌注损伤挽救激酶（风险）途径]和STAT3 [幸存者激活因子增强（安全）途径]通过Western印迹分析确定。 Wortmannin / U0126或AG490分别用于药理学风险或安全封锁。猪血浆/等离子体透析液分别取样，分别转移到分离的大鼠和小鼠心脏后30分钟/ 120分钟的全球缺血再灌注。在早期再灌注，从大鼠心中分离了线粒体。孤立的鼠标心肌细胞对缺氧/ 5分钟的再氧化而没有并且具有先前的等离子体透析液孵育。粉体在PLA的猪中减少了婴儿的梗塞大小与PLA的44±9％（风险面积的面积百分比，平均值？±SD，P <0.05）和早期再灌注增加的STAT3磷酸化。 AG490但没有风险阻止保护。朗科血浆/等离子体透析液在大鼠中减少梗塞大小（22±3％的心室质量与PLA等离子体，P <0.05）和小鼠（29±4％与63±8％）（29±4％） PLA等离子体透析液，P <0.05）心脏和改善的线粒体功能（例如，增加呼吸，ATP形成和钙保留容量和反应性氧物种形成减少）。 RPER透析液还改善了缺氧/再氧化后小鼠心肌细胞的活力。风险或安全封锁每个人废除了这些有益的效果。新的和值得注意的远程缺血性令急性梗死患者心肌的挽救。我们鉴定了猪体液转移和STAT3活化的信号转导和再灌注损伤激酶和DAT3在大鼠和小鼠心中的参与，以及更好的心肌细胞活力和线粒体功能。

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