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The co-application of hypoxic preconditioning and postconditioning abolishes their own protective effect on systolic function in human myocardium

机译:低氧预适应和后适应的共同应用消除了它们自身对人心肌收缩功能的保护作用

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Background: Ischemic preconditioning (IPC) and postconditioning (POC) are well documented to trigger cardioprotection against ischemia/reperfusion (I/R) injury, but the effect oftheir both co-application remains unclear in human heart. The present study sought to assessthe co-application of IPC and POC on fragments of human myocardium in vitro.Methods: Muscular trabeculae of the human right atrial were electrically driven in the organbath and subjected to simulated I/R injury – hypoxia/re-oxygenation injury in vitro. To achieveIPC of trabeculae the single brief hypoxia period preceded the applied lethal hypoxia, and to achieve POC triple brief hypoxia periods followed the lethal hypoxia. Additional muscular trabeculae were exposed only to the hypoxic stimulation (Control) or were subjected to the non-hypoxic stimulation (Sham). 10 μM norepinephrine (NE) application ended every experiment to assess viability of trabeculae. The contraction force of the myocardium assessed as a maximal amplitude of systolic peak (%Amax) was obtained during the whole experiment’s period.Results: Co-application of IPC and POC resulted in decrease in %Amax during the re-oxygentaionperiod and after NE application, as compared to Control (30.35 ± 2.25 vs. 41.89 ± 2.25, 56.26 ± 7.73 vs. 65.98 ± 5.39, respectively). This was in contrary to the effects observed when IPC and POC were applied separately.Conclusions: The co-application of IPC and POC abolishes the cardioprotection of either intervention alone against simulated I/R injury in fragments of the human right heart atria.
机译:背景:缺血预适应(IPC)和后适应(POC)可以触发针对缺血/再灌注(I / R)损伤的心脏保护作用,但在人的心脏中,两者的共同应用尚不清楚。本研究旨在评估IPC和POC在体外对人体心肌碎片的共同应用。方法:将右心房肌小梁在器官浴中电动驱动,并遭受模拟的I / R损伤–缺氧/再充氧体外损伤。为了实现小梁的IPC,在施加致命性缺氧之前先进行短暂的短暂缺氧,然后在致死性缺氧之后达到POC三次短暂缺氧。仅将另外的肌肉小梁暴露于低氧刺激下(对照)或进行非低氧刺激(假手术)。 10μM去甲肾上腺素(NE)的应用结束了每个实验以评估小梁的生存能力。在整个实验过程中,获得的心肌收缩力被评估为收缩期峰的最大振幅(%A max )。结果:IPC和POC的共同应用导致%A <与对照相比,在补氧期间和应用NE后的sub> max (分别为30.35±2.25和41.89±2.25、56.26±7.73和65.98±5.39)。这与单独使用IPC和POC时观察到的效果相反。结论:IPC和POC的共同应用取消了任何一种干预措施对单独的右心房心房中模拟I / R损伤的心脏保护作用。

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