Does delayed no-reflow phenomenon cause myocardial necrosis?
Abstract Although recent studies have suggested that the no-reflow region progressively extends during the later reperfusion period, whether this “delayed” no-reflow causes myocardial necrosis remains unknown. To examine this question, we analyzed alteration of the size and histology of the no-reflow region and regional contractlie function after ischemia/reperfusion in anesthesized rabbit preparation. The no-reflow zone after 30-minute ischemia was 13.3 ± 4.2% of the ischemic region at 10 minutes after reperfusion and 35.1 ± 6.4% at 60 minutes, which indicates a significant extension of the no-reflow region during a 60-minute reperfusion period. There were both almost-normal-appearing myovytes and necrotic cells with contraction bands in the no-reflow zone at 10 minutes after reperfusion. In contrast, the larger region of no-reflow region after a 60-minute reperfusion consisted mostly of contraction band necrosis, suggesting irreversible ischemic cell injury in this area before reflow. The regional systolic thickening fraction (TF), which was reduced to −86 ± 23% after 30-minute ischemia, recovered to −30 ± 20% of the baseline value after 10 minutes of reperfusion, and there was no deterioration in the TF during the subsequent reperfusion. Furthermore, the response of TF to dobutamine (5 and 10 μ g/kg/min, i.v.), which was infused to eliminate myocardial stunning, did not decrease during the 60-minute reperfusion period. These results suggest that delayed no-reflow does not extend myocardial infarction.