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首页> 外文期刊>American Journal of Physiology >Pyruvate-fortified cardioplegia suppresses oxidative stress and enhances phosphorylation potential of arrested myocardium.
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Pyruvate-fortified cardioplegia suppresses oxidative stress and enhances phosphorylation potential of arrested myocardium.

机译：丙酮酸增强的心脏停搏可以抑制氧化应激并增强被捕心肌的磷酸化潜能。

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摘要

Cardioplegic arrest for bypass surgery imposes global ischemia on the myocardium, which generates oxyradicals and depletes myocardial high-energy phosphates. The glycolytic metabolite pyruvate, but not its reduced congener lactate, increases phosphorylation potential and detoxifies oxyradicals in ischemic and postischemic myocardium. This study tested the hypothesis that pyruvate mitigates oxidative stress and preserves the energy state in cardioplegically arrested myocardium. In situ swine hearts were arrested for 60 min with a 4:1 mixture of blood and crystalloid cardioplegia solution containing 188 mM glucose alone (control) or with additional 23.8 mM lactate or 23.8 mM pyruvate and then reperfused for 3 min with cardioplegia-free blood. Glutathione (GSH), glutathione disulfide (GSSG), and energy metabolites [phosphocreatine (PCr), creatine (Cr), P(i)] were measured in myocardium, which was snap frozen at 45 min arrest and 3 min reperfusion to determine antioxidant GSH redox state (GSH/GSSG) and PCrphosphorylation potential {[PCr]/([Cr][P(i)])}. Coronary sinus 8-isoprostane indexed oxidative stress. Pyruvate cardioplegia lowered 8-isoprostane release approximately 40% during arrest versus control and lactate cardioplegia. Lactate and pyruvate cardioplegia dampened (P < 0.05 vs. control) the surge of 8-isoprostane release following reperfusion. Pyruvate doubled GSH/GSSG versus lactate cardioplegia during arrest, but GSH/GSSG fell in all three groups after reperfusion. Myocardial [PCr]/([Cr][P(i)]) was maintained in all three groups during arrest. Pyruvate cardioplegia doubled [PCr]/([Cr][P(i)]) versus control and lactate cardioplegia after reperfusion. Pyruvate cardioplegia mitigates oxidative stress during cardioplegic arrest and enhances myocardial energy state on reperfusion.
机译：旁路手术的心脏停搏会在心肌上造成局部缺血，从而产生氧自由基并消耗心肌高能磷酸盐。糖酵解代谢物丙酮酸而不是其还原的同类乳酸，增加了磷酸化的潜力，并使缺血性和缺血后心肌中的氧自由基解毒。这项研究检验了丙酮酸减轻氧化应激并保留心律失常的心肌中能量状态的假说。用血液和仅含有188 mM葡萄糖的葡萄糖和结晶性心脏停搏液的4：1混合物（对照）或另外的23.8 mM乳酸或23.8 mM丙酮酸将原位猪心脏停搏60分钟，然后用无心脏停搏的血液再灌注3分钟。在心肌中测量了谷胱甘肽（GSH），二硫谷胱甘肽（GSSG）和能量代谢物[磷酸肌酸（PCr），肌酸（Cr），P（i）]，将其速冻45分钟后再冷冻，再灌注3分钟以测定抗氧化剂GSH氧化还原态（GSH / GSSG）和PCr磷酸化电位{[PCr] /（[[Cr] [P（i）]）}}。冠状窦8异前列腺素索引的氧化应激。相对于对照和乳酸性心脏停搏，丙酮酸心脏停搏降低了8-异前列腺素的释放。乳酸和丙酮酸心脏停搏可减轻（相对于对照组，P <0.05）再灌注后8-异前列腺素释放的高峰。在停搏期间，丙酮酸丙酮酸使GSH / GSSG相对于乳酸性心脏停搏增加了一倍，但三组中的GSH / GSSG在再灌注后均下降。逮捕期间所有三组均维持心肌[PCr] /（[[Cr] [P（i）]）。丙酮酸心脏停搏[PCr] /（[[Cr] [P（i）]）比对照和乳酸心脏停搏加倍。丙酮酸心麻痹减轻心脏停搏时的氧化应激，并增加再灌注时的心肌能量状态。

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