Koomen J M, Schevers J A, Noordhoek J, Zimmerman A N
Basic Res Cardiol. 1983 Mar-Apr;78(2):227-38. doi: 10.1007/BF01906675.
The effects of omission of Mg2+ during Ca2+-free perfusion (3 min) of either spontaneously beating and electrically stimulated rat hearts were studied. Ca2+-free perfusion per se induced cardiac arrest and coronary vasodilation, and increased intrinsic pulse rate of the heart. Upon reperfusion with Ca2+, cardiac function was lost and parallelled by a sudden and massive release of cellular constituents ("calcium paradox"). Mg2+-free perfusion evoked effects opposite from Ca2+-free, with exception of heart rate which was increased. During Ca2+-Mg2+-free perfusion the electrocardiogram became irregular within 30 s, and this effect was followed by transient "spasmodic contractions". The effects of normal reperfusion were indistinguishable from those observed after Ca2+-free perfusion in the presence of Mg2+. Addition of Mn2+ or La3+ to the Ca2+-Mg2+-free perfusion medium completely inhibited the induction of electrical irregularities and spasmodic contractions. The typical effects of Ca2+-Mg2+-free perfusion are discussed in terms of Mg-Ca and Mg-K interactions at the sarcolemmal surface. It was concluded that our results may contribute indirectly to an explanation of the protective effect of high Mg2+-concentrations during Ca2+-free as well as ischemic perfusion of mammalian hearts.
研究了在无钙灌注(3分钟)期间省略镁离子对自发搏动和电刺激大鼠心脏的影响。无钙灌注本身会导致心脏骤停和冠状动脉舒张,并增加心脏的固有心率。在用钙离子再灌注时,心脏功能丧失,同时伴随着细胞成分的突然大量释放(“钙反常”)。除了心率增加外,无镁灌注产生的效应与无钙灌注相反。在无钙无镁灌注期间,心电图在30秒内变得不规则,随后出现短暂的“痉挛性收缩”。正常再灌注的效应与在有镁存在的情况下无钙灌注后观察到的效应无法区分。向无钙无镁灌注培养基中添加锰离子或镧离子完全抑制了电不规则性和痉挛性收缩的诱导。从肌膜表面的镁-钙和镁-钾相互作用方面讨论了无钙无镁灌注的典型效应。得出的结论是,我们的结果可能间接地有助于解释高镁浓度在无钙以及哺乳动物心脏缺血灌注期间的保护作用。