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首页> 外文期刊>American Journal of Physiology >The intermediary metabolite pyruvate attenuates stunning and reduces infarct size in in vivo porcine myocardium.
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The intermediary metabolite pyruvate attenuates stunning and reduces infarct size in in vivo porcine myocardium.

机译：中间代谢产物丙酮酸减弱了体内猪心肌中的击晕并减小了梗塞面积。

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The intermediary metabolite pyruvate has been shown to exert significant beneficial effects in in vitro models of myocardial oxidative stress and ischemia-reperfusion injury. However, there have been few reports of the ability of pyruvate to attenuate myocardial stunning or reduce infarct size in vivo. This study tested whether supraphysiological levels of pyruvate protect against reversible and irreversible in vivo myocardial ischemia-reperfusion injury. Anesthetized, open-chest pigs (n = 7/group) underwent 15 min of left anterior descending coronary artery (LAD) occlusion and 3 h of reperfusion to induce stunning. Load-insensitive contractility measurements of regional preload recruitable stroke work (PRSW) and PRSW area (PRSWA) were generated. Vehicle or pyruvate (100 mg/kg i.v. bolus + 10 mg x kg(-1) x min(-1) intra-atrial infusion) was administered during ischemia and for the first hour of reperfusion. In infarct studies, pigs (n = 6/group) underwent 1 h of LAD ischemia and 3 h of reperfusion. Group I pigs received vehicle or pyruvate for 30 min before and throughout ischemia. In group II, the infusion was extended through 1 h of reperfusion. In the stunning protocol, pyruvate significantly improved the recovery of PRSWA at 1 h (50 +/- 4% vs. 23 +/- 3% in controls) and 3 h (69 +/- 5% vs. 39 +/- 3% in controls) reperfusion. Control pigs exhibited infarct sizes of 66 +/- 1% of the area at risk. The pyruvate I protocol was associated with an infarct size of 49 +/- 3% (P < 0.05), whereas the pyruvate II protocol was associated with an infarct size of 30 +/- 2% (P < 0.05 vs. control and pyruvate I). These findings suggest that pyruvate attenuates stunning and decreases myocardial infarction in vivo in part by reduction of reperfusion injury. Metabolic interventions such as pyruvate should be considered when designing the optimal therapeutic strategies for limiting myocardial ischemia-reperfusion injury.
机译：中间体丙酮酸丙酮酸酯已显示在心肌氧化应激和局部缺血-再灌注损伤的体外模型中发挥重要的有益作用。然而，几乎没有关于丙酮酸在体内减弱心肌电击或减小梗塞面积的能力的报道。这项研究测试了丙酮酸的超生理水平是否可以预防体内心肌缺血-再灌注损伤的可逆和不可逆。麻醉的开胸猪（n = 7 /组）左冠状动脉左前降支（LAD）阻塞15分钟，再灌注3 h引起惊厥。生成了对区域预负荷可招募中风工作（PRSW）和PRSW区域（PRSWA）的不敏感负荷的收缩力测量。在局部缺血和再灌注的第一小时内，施用媒介物或丙酮酸盐（100 mg / kg静脉推注+ 10 mg x kg（-1）x min（-1）心房内输注）。在梗塞研究中，猪（n = 6 /组）进行了1小时的LAD缺血和3小时的再灌注。第一组猪在局部缺血之前和整个过程中接受媒介物或丙酮酸30分钟。在第二组中，输注持续了1小时。在令人惊叹的实验方案中，丙酮酸显着改善了1小时（50 +/- 4％比对照组的23 +/- 3％）和3小时（69 +/- 5％比39 +/- 3）的PRSWA回收率。对照组）。对照猪的梗塞面积占危险区域的66 +/- 1％。丙酮酸I方案的梗死面积为49 +/- 3％（P <0.05），而丙酮酸II方案的梗死面积为30 +/- 2％（与对照和丙酮酸相比，P <0.05一世）。这些发现表明，丙酮酸减弱了体内的再灌注损伤，从而减轻了体内的电击感并减少了心肌梗塞。在设计限制心肌缺血-再灌注损伤的最佳治疗策略时，应考虑采用丙酮酸等代谢干预措施。

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