Reactive oxygen species (ROS) have been implicated in the mechanism of postischemic contractile dysfunction, known as myocardial stunning. In this study, we examined protective effects of antioxidant enzymes, superoxide dismutase (SOD) and catalase, against ischemia/reperfusion-induced cardiac dysfunction and inhibition of Na+,K+-ATPase activity. Isolated Langendorff-perfused rabbit hearts were subjected to 15 min of global normothermic ischemia followed by 10 min reperfusion. The hearts treated with SOD plus catalase did not show significant recovery of left ventricular (LV) end-diastolic pressure compared with untreated ischemic reperfused hearts. Treatment with antioxidants had no protective effects on developed LV pressure or its maximal positive and negative first derivatives (±LVdP/dt). Myocardial stunning was accompanied by significant loss in sarcolemmal Na+,K+-ATPase activity and thiol group content. Inhibition of enzyme activity and oxidation of SH groups were not prevented by antioxidant enzymes. These results suggest that administration of SOD and catalase in perfusate do not protect significantly against cardiac dysfunction in stunned rabbit myocardium., P. Kaplán, M. Matejovičová, P. Herijgers, W. Flameng., and Obsahuje bibliografii a bibliografické odkazy
In the myocardium, the sarcoplasmic reticulum (SR) plays an essential role in the regulation of cytosolic free Ca2 + ion concentration and, hence, in the contraction-relaxation cycle. The aim of this review is to summarize the role of the SR, particularly the main SR Ca2+ transport proteins, Ca2+-ATPase pump and Ca2+ release channel (ryanodine receptor), in contractile impairment during ischaemia and reperfusion. As suggested by most studies, SR dysfunction may contribute to contractile failure during ischaemia. However, SR function is largely restored during reperfusion and minor changes are unlikely to explain the severe postischaemic contractile dysfunction.