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首页> 外文期刊>Cellular Physiology and Biochemistry >The cardioprotective effect of brief acidic reperfusion after ischemia in perfused rat hearts is not mimicked by inhibition of the Na~+/H ~+ exchanger NHE1
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The cardioprotective effect of brief acidic reperfusion after ischemia in perfused rat hearts is not mimicked by inhibition of the Na~+/H ~+ exchanger NHE1

机译：Na〜+ / H〜+交换子NHE1的抑制作用不能模拟缺血后短暂的酸性再灌注对心脏的保护作用。

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摘要

Ischemic postconditioning (PostC), i.e. brief ischemia-reperfusion cycles before full reperfusion, is protective against cardiac ischemia/reperfusion (I/R) injury. Inhibition of the Na ~+/H~+ exchanger NHE1 and delayed intracellular pH-normalization have been proposed to underlie protection by PostC. Methods and Results: We used Langendorff perfused rat hearts exposed to 35 min global ischemia to show that 15 min acidic (pH 6.5) treatment at onset of reperfusion decreased infarct size and functional deterioration at least to the same extent as PostC. In contrast, NHE1 inhibition by EIPA was detrimental. To evaluate HL-1 atrial cardiomyocytes as a cellular model for PostC, we exposed the cells to simulated ischemia/reperfusion (I/R) mimicking that in perfused hearts. Necrosis and apoptosis induced by I/R were unaffected by 15 min of pH 6.0 at onset of reperfusion. I/R increased the activity of c-Jun N-terminal Kinase 1/2 (JNK1/2) and Akt, but not of p38 MAPK, with no further effect of acidic reperfusion or EIPA. Conclusion: In rat hearts, 15 min acidic reperfusion improves myocardial performance at least as much as does PostC, whereas NHE1 inhibition is detrimental. In contrast, in HL-1 cardiomyocytes, acidic reperfusion or NHE1 inhibition affect neither survival nor JNK1/2-, Akt-, and p38 MAPK activity after I/R, pointing to different mechanisms of damage and protection in these systems.
机译：缺血后处理（PostC），即完全再灌注前的短暂缺血-再灌注周期可防止心脏缺血/再灌注（I / R）损伤。已提出抑制Na〜+ / H〜+交换子NHE1和延迟细胞内pH归一化是PostC保护的基础。方法和结果：我们使用暴露于35分钟整体缺血的Langendorff灌注大鼠心脏，显示在再灌注开始时进行15分钟的酸性（pH 6.5）治疗可减少梗死面积和功能恶化，其程度至少与PostC相同。相反，EIPA对NHE1的抑制作用是有害的。为了评估HL-1心房心肌细胞作为PostC的细胞模型，我们将细胞暴露于模拟的缺血/再灌注（I / R）中，模拟的是在灌注心脏中的缺血/再灌注。再灌注开始时，pH 6.0的15分钟不会影响I / R引起的坏死和凋亡。 I / R增加c-Jun N末端激酶1/2（JNK1 / 2）和Akt的活性，但不增加p38 MAPK的活性，而没有酸性再灌注或EIPA的进一步作用。结论：在大鼠心脏中，15分钟的酸性再灌注至少可以改善PostC的心肌功能，而NHE1的抑制作用是有害的。相反，在HL-1心肌细胞中，酸性再灌注或NHE1抑制既不影响生存，也不影响I / R后的JNK1 / 2-，Akt-和p38 MAPK活性，这表明这些系统中不同的损伤和保护机制。

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