Elmoselhi A, Butcher A, Samson S E, Grover A K
Department of Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada.
Gen Physiol Biophys. 1994 Jun;13(3):247-56.
Oxygen radicals accumulated during ischemia and reperfusion may affect coronary contractility by endothelium dependent and independent pathways one of which may involve Na(+)-pump. Here we report a contractility assay for Na(+)-pump in pig coronary artery and use it to examine the effects of hydrogen peroxide and superoxide. Coronary artery rings contracted in a K(+)-free Krebs solution and relaxed upon subsequent exposure to K+. The relaxation approximated a single exponential decay whose rate constant depended on [K+]2. This K(+)-induced relaxation was abolished by ouabain and was attributed to Na(+)-pump. In tissues pretreated with peroxide, the rate of relaxation of the K(+)-free contracted arteries decreased with an IC50 = 1.6 +/- 0.6 mmol/l for peroxide. Another set of tissues was pretreated with the superoxide generating system containing 0.3 mmol/l xanthine + varying concentrations of xanthine oxidase (XO) and precontracted in K(+)-free Krebs solution. The rate of the K(+)-induced relaxation decreased with IC50 = 24 +/- 8 mU/ml for XO. Thus, using the relaxation assay we conclude that exposing coronary arteries to oxygen radicals can damage Na(+)-pumps.
缺血和再灌注过程中积累的氧自由基可能通过内皮依赖和非依赖途径影响冠状动脉收缩性，其中一条途径可能涉及钠泵。在此，我们报告一种猪冠状动脉钠泵收缩性测定方法，并利用它来检测过氧化氢和超氧化物的作用。冠状动脉环在无钾的Krebs溶液中收缩，随后暴露于钾离子时松弛。这种松弛近似于单指数衰减，其速率常数取决于[K⁺]²。这种钾离子诱导的松弛被哇巴因消除，并归因于钠泵。在用过氧化物预处理的组织中，无钾收缩动脉的松弛速率降低，过氧化物的半数抑制浓度（IC50）为1.6±0.6 mmol/L。另一组组织用含有0.3 mmol/L黄嘌呤+不同浓度黄嘌呤氧化酶（XO）的超氧化物生成系统预处理，并在无钾的Krebs溶液中预收缩。钾离子诱导的松弛速率降低，XO的IC50为24±8 mU/ml。因此，通过松弛测定，我们得出结论，使冠状动脉暴露于氧自由基会损害钠泵。
