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首页> 外文期刊>American Journal of Physiology >Long-term infusion of Met5-enkephalin fails to protect murine hearts against ischemia-reperfusion injury.
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Long-term infusion of Met5-enkephalin fails to protect murine hearts against ischemia-reperfusion injury.

机译：长期输注Met5-脑啡肽不能保护鼠心免受缺血-再灌注损伤。

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摘要

Recently, we reported that exogenous administration of Met(5)-enkephalin (ME) for 24 h reduces infarct size after ischemia-reperfusion in rabbits. In the present study, we tested whether ME-induced cardioprotection is exhibited in murine hearts and whether chronic infusion of this peptide can render hearts tolerant to ischemia. Barbiturate-anesthetized open-chest mice (C57BL/6J) were subjected to regional myocardial ischemia-reperfusion (45 min of occlusion and 20 min of reperfusion). Mice received saline vehicle or ME for 24 h or 2 wk before undergoing regional myocardial ischemia-reperfusion or for 24 h followed by a 24-h delay before regional myocardial ischemia-reperfusion. Infarct size was measured with propidium iodide and is expressed as a percentage of the area at risk. Infarcts were smaller after infusion of ME for 24 h than with vehicle control: 49.2 +/- 9.0% vs. 22.2 +/- 3.2% (P < 0.01). In contrast, administration of ME for 2 wk failed to elicit cardioprotection: 36.5 +/- 9.1% and 41.4 +/- 8.2% for control and ME, respectively (P = not significant). When a 24-h delay was imposed between the end of drug treatment and the onset of the ischemic insult, cardioprotection was lost: 38.5 +/- 6.1% and 42.8 +/- 6.6% for control and ME, respectively (P = not significant). Chronic sustained exogenous infusion of the endogenously produced opioid peptide ME is associated with loss of the cardioprotection that is observed with 24 h of infusion. Furthermore, in this in vivo murine model, ME failed to induce delayed tolerance to myocardial ischemia-reperfusion.
机译：最近，我们报道外源给药Met（5）-脑啡肽（ME）24小时减少了兔缺血再灌注后的梗塞面积。在本研究中，我们测试了在小鼠心脏中是否表现出ME诱导的心脏保护作用，以及长期输注该肽是否可以使心脏耐受局部缺血。接受巴比妥酸盐麻醉的开胸小鼠（C57BL / 6J）进行局部心肌缺血再灌注（闭塞45分钟，再灌注20分钟）。在进行局部心肌缺血-再灌注之前，小鼠接受了24h或2 wk的生理盐水或ME的治疗，或者在进行局部心肌缺血-再灌注之前延迟了24 h，然后接受了24 h的延迟。用碘化丙锭测量梗塞面积，并表示为危险区域的百分比。输注ME 24小时后的梗死面积比溶媒对照组小：49.2 +/- 9.0％与22.2 +/- 3.2％（P <0.01）。相比之下，连续2周服用ME未能引起心脏保护：对照组和ME分别为36.5 +/- 9.1％和41.4 +/- 8.2％（P =不显着）。在药物治疗结束与缺血性发作发作之间延迟24小时后，心脏保护功能丧失：对照和ME分别为38.5 +/- 6.1％和42.8 +/- 6.6％（P =不显着） ）。内源性阿片肽ME的长期持续外源性输注与24 h输注时观察到的心脏保护功能丧失有关。此外，在该体内鼠模型中，ME未能诱导对心肌缺血-再灌注的延迟耐受。

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