Although recent studies have suggested that the no-reflow region progr
essively extends during the later reperfusion period, whether this ''d
elayed'' no-reflow causes myocardial necrosis remains unknown. To exam
ine this question, we analyzed alteration of the size and histology of
the no-reflow region and regional contractile function after ischemia
/reperfusion in anesthetized rabbit preparation. The no-reflow zone af
ter 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 indic
ates a significant extension of the no-reflow region during a 60-minut
e reperfusion period. There were both almost-normal-appearing myocytes
and necrotic cells with contraction bands in the no-reflow zone at 10
minutes after reperfusion. In contrast, the larger region of no-reflo
w region after a 60-minute reperfusion consisted mostly of contraction
band necrosis, suggesting irreversible ischemic cell injury in this a
rea before reflow. The regional systolic thickening fraction (TF), whi
ch 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 mu g/kg/min,
i.v.), which was infused to eliminate myocardial stunning, did not de
crease during the 60-minute reperfusion period. These results suggest
that delayed no-reflow does not extend myocardial infarction.