Jynge P
Thorac Cardiovasc Surg. 1980 Oct;28(5):303-9. doi: 10.1055/s-2007-1022100.
Studies in the globally ischemic, isolated rat heart have shown that the preischemic coronary infusion of calcium-free cardioplegic solution may lead to an exacerbation of the postischemic leakage of creatine kinase. This exacerbation could be prevented by the inclusion of trace amounts of calcium in the coronary infusate or could be postponed by the omission of calcium during postischemic reperfusion. The calcium paradox, observed with such a combination of coronary infusion and ischemia required for its induction a less extensive cellular calcium depletion than that induced by infusion only and was the result of 2 additive factors: the washout of tissue calcium during preischemic infusion and the cellular influx of residual membrane-bound calcium during ischemia. The balance between protective and damaging properties with calcium-free cardioplegic infusates was influenced by the concentration of Na+, K+, Mg++ and procaine in the infusates as these agents influence patterns of calcium redistribution.
对全球缺血的离体大鼠心脏的研究表明,缺血前冠状动脉输注无钙心脏停搏液可能会导致缺血后肌酸激酶漏出加剧。通过在冠状动脉灌注液中加入微量钙可预防这种加剧,或者通过在缺血后再灌注期间不加入钙可将其推迟。钙反常现象,在这种冠状动脉灌注和诱导其所需的缺血的组合中观察到,与仅通过灌注诱导的相比,其诱导所需的细胞钙耗竭程度较小,并且是两个相加因素的结果:缺血前灌注期间组织钙的洗脱以及缺血期间残余膜结合钙的细胞内流入。无钙心脏停搏灌注液的保护和损伤特性之间的平衡受灌注液中Na+、K+、Mg++和普鲁卡因浓度的影响,因为这些物质会影响钙再分布模式。