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心脏富氧灌流30min稳定后随机分为四组:(1)对照组:富氧灌流75min;(2)低血流缺氧组:低血流缺氧45min后,再富氧灌流30min;(3)Ouabain组:于低血流缺氧过程中,溶Ouabain(200μmol/L)于K—H液中,余同组(2);(4)Ouabain+Amiloride组:除在低血流缺氧期给0.5mmol/L amiloride外,余同组(3)。与低血流缺氧组相比,Ouabain可引起再灌注时心肌Na的明显增加并伴有心室功能的抑制,Amiloride可明显减轻这一损害作用。这表明,Na/K ATPase活性的抑制与再灌注心肌的Na超载有关,而这一作用的机制可能是由于Na/H交换的激活所引起。
(2) Hypoxia and hypoxia group: After hypoxia and hypoxia for 45min, reoxygenated perfusion was performed for 30min; (3) ) Ouabain group: Ouabain (200μmol / L) was dissolved in K-H solution during hypoxemia and hypoxia, the rest of the same group (2); (4) Ouabain + Amiloride group: To 0.5mmol / L amiloride outside, the same group (3). Compared with hypoxemia and hypoxia groups, Ouabain induced markedly increased myocardial Na with reperfusion and ventricular dysfunction, and Amiloride significantly reduced this damage. This indicates that the inhibition of Na / K ATPase activity is related to Na overload in reperfused myocardium, and the mechanism of this effect may be due to the activation of Na / H exchange.