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The Heart Institute, Good Samaritan Hospital, University of Southern California, Los Angeles, California 90017-2395
The aim was to define the degree and time
course of reperfusion-related expansion of no reflow. In five groups of
anesthetized, open-chest rabbits (30-min coronary occlusion and
different durations of reperfusion), anatomic no reflow was determined
by injection of thioflavin S at the end of reperfusion and compared
with regional myocardial blood flow (RMBF; radioactive microspheres)
and infarct size (triphenyltetrazolium). The area of no reflow
progressively increased from 12.2 ± 4.2% of the risk area after
2 min of reperfusion to 30.8 ± 3.1% after 2 h and 34.9 ± 3.3% after 8 h and significantly correlated with infarct size
after 1 h of reperfusion (r = 0.88-0.97). This rapid expansion of no reflow predominantly occurred during the
first 2 h, finally encompassing ~80% of the infarct size, and
was accompanied by a decrease of RMBF within the risk area, being
hyperemic after 2 min of reperfusion (3.78 ± 0.75 ml · min
1 · g1) and
plateauing at a level of ~0.9
ml · min1 · g1 by 2 and
8 h of reperfusion (preischemic RMBF: 2.06 ± 0.01 ml · min1 · g1). The
development of macroscopic hemorrhage lagged behind no reflow, was
closely correlated with it, and may be the consequence of microvascular damage.
myocardial infarction; microcirculation; vasculature; hemorrhage
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