The effects of ruthenium red on mitochondrial function during post-ischaemic reperfusion

Recently several attempts have been made to reduce reperfusion-induced calcium accumulation in the myocardium and in the mitochondria by using inhibitors of slow channel calcium transport such as verapamil, nifedipine and diltiazem. When these substances were given to the animals before death, or at the onset of ischaemia, they have been shown to prevent calcium accumulation in whole tissue and in isolated mitochondria [7–9, 15], while when added at the time of reperfusion, they failed to prevent myocardial calcium overloading [3, 15]. This supports the view that reperfusion-induced tissue calcium accumulation does not necessarily occur through the slow calcium channels and, at the present, the cause and the way in which this phenomenon can be modified by pharma-cological or other interventions remains unclear.For this reason, in this present study, we used ruthenium red in an attempt to reduce directly the reperfusion-induced mitochondrial calcium accumulation. Ruthenium is a polysaccaride dye which specifically inhibits calcium transport and binding by liver and heart mitochondria [7, 11].