摘要
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。
Thirty min affer stabilization perfusion with oxygenated buffer, hearts weredivided in four groups: (1) Control group: 75 min. of aerobic perfusion; (2) Lowflow anoxia group: 45 min. of low flow anoxio perfusion (95% N_2:5%CO_2, 0.15ml/min.) followed by 30 min. of aerobic perfusion; (3) Ouabain group: protocolsame as (2), except that ouabain(200 μmol/L) was added to anoxic perfusate duringlow flow anoxia; (4) Ouabain+Amiloride group: protocol same as (3) except thatamiloride (0.5 mmol/I) was added to perfusate during low flow anoxia. Com-pared with the low now anoxia group, ouabain resulted in an additional increarsein Na during reperfusion accompanied with a depressed ventricular function.The deleterious effects of ouabain could be significantly combated by amiloride.It is concluded that a decrease in Na/K ATP ase activity may contribute to Na gainin reperfused myocardium, the mechanism of which might result from stimulation ofNa/H exchange.
出处
《生理学报》
CAS
CSCD
北大核心
1992年第5期510-514,共5页
Acta Physiologica Sinica