Hugtenburg J G, Van Voorst M J, Van Marle J, Mathy M J, Beckeringh J J, Van Veen H A, Hendriks M G, Van Zwieten P A
Department of Pharmacotherapy/Pharmacology, Faculty of Medicine, University of Amsterdam, The Netherlands.
Eur J Pharmacol. 1990 Mar 13;178(1):71-8. doi: 10.1016/0014-2999(90)94794-x.
The influence of nifedipine (20 nM) and mioflazine (300 nM), i.e. concentrations inducing a 60-70% recovery of cardiac function during reperfusion of globally ischaemic guinea-pig working hearts, on the mitochondrial calcium content was investigated in normoxic, globally ischaemic and reperfused globally ischaemic guinea-pig working hearts. Mitochondrial calcium was determined electronmicroscopically with oxalate-pyroantimonate method. In normoxic hearts both nifedipine and mioflazine reduced the mitochondrial calcium content. Global ischaemia for 45 min and subsequent reperfusion for 25 min resulted in a pronounced mitochondrial calcium overload and damage to the cellular structure. In ischaemic and in reperfusion hearts the drugs maintained mitochondrial calcium at pre-ischaemic levels and decreased the damage to the cellular structure.
研究了硝苯地平(20纳摩尔)和米氟嗪(300纳摩尔),即在全缺血豚鼠工作心脏再灌注期间诱导心脏功能恢复60 - 70%的浓度,对常氧、全缺血及再灌注的全缺血豚鼠工作心脏线粒体钙含量的影响。采用草酸 - 焦锑酸盐法通过电子显微镜测定线粒体钙含量。在常氧心脏中,硝苯地平和米氟嗪均降低了线粒体钙含量。45分钟的全缺血及随后25分钟的再灌注导致明显的线粒体钙超载和细胞结构损伤。在缺血和再灌注心脏中,这些药物使线粒体钙维持在缺血前水平,并减少了对细胞结构的损伤。