Abstract
We have examined the role of readmission of oxygen in the initiation of reperfusion-induced arrhythmias by separating readmission flow from readmission of oxygen on a temporal basis. Isolated rat hearts (n=12/group) were subjected to 10 minutes of global ischemia and reperfusion. In controls reperfused with aerobic perfusion medium, 100% of hearts developed ventricular tachycardia 1.48±0.78 seconds after reperfusion, and ventricular fibrillation occurred 13.47±2.91 seconds after reperfusion. Also in hearts reperfused with anoxic perfusion medium, 100% of hearts developed ventricular tachycardia 1.98±0.96 seconds after reperfusion, and ventricular fibrillation occurred 27.01±18.52 seconds after reperfusion. But the duration of the time from reperfusion to the onset of ventricular fibrillation were statistically differrent in these two groups (p<0.05). In conclusion anoxic reperfusion delayed ventricular fibrillation but prevent neither ventricular fibrillation nor ventricular tachycardia. This implies that oxygen-derived free radicals may play an important role in the initiation of reperfusion-induced arrhythmias, but are unneccessary for arrhythmogenesis.
