Résumé
It is currently believed that reperfusion injury of the ischemic or hypoxic myocardium can be attributed, at least in part, to an overproduction of reactive oxygen species (ROS). The aim of the present study was to determine whether ischemia (of different severity or duration) followed by reperfusion can affect the activity of endogenous scavenger enzymes in isolated perfused rat hearts.
Isolated Langendorff perfused rat hearts were subjected to either total (10, 20 or 30 min; zero-flow) or partial (30, 60 or 90 min; low-flow of 0.10 or 0.35 ml/min) ischemia, followed by 10 min of reperfusion. Enzymatic activities of total superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) were determined in cardiac tissues at the end of the perfusion protocol.
Basal scavenger enzyme activities measured in control hearts (perfused under normoxic conditions) were 33.90 ± 4.88, 31.20 ± 5.32 and 1.61 ± 0.29 IU/mg protein (mean ± SD,
n = 6 per group) for SOD, catalase and GPx respectively. Our results indicate that neither total SOD, GPx, nor catalase myocardial activities were changed whatever the perfusion protocol followed.
The present study shows that the endogenous pool of catalytic ROS scavengers is not dramatically altered during ischemia or upon reperfusion. This suggests that ROS scavengers are not directly involved in the development of ischemia/reperfusion injuries. These results also support the premise that excessive radical generation does not occur in this model, where the isolated heart is subjected to ischemia.