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Articles in PresS, published online ahead of print May 23, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00270.2002
Submitted on March 28, 2002
Accepted on May 6, 2002
1 The Heart Institute, University of Southern California, Good Samaritan Hospital, Los Angeles, California, USA
* To whom correspondence should be addressed. E-mail: RKloner{at}goodsam.org.
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 minutes 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 two minutes of reperfusion to 30.8±3.1% after 2 hours and 34.9±3.3% after 8 hours, and significantly correlated with infarct size after one hour of reperfusion (r=0.88-0.97). This rapid expansion of no-reflow predominantly occurred during the first two hours, finally encompassing about 80% of infarct size, and was accompanied by a decrease of RMBF within the risk area, being hyperemic after two minutes of reperfusion (3.78±2.25 ml/min/g) and plateauing at a level of about 0.9 ml/min/g by 2 and 8 hours of reperfusion. (preischemic RMBF 2.06±0.01 ml/min/g). The development of macroscopic hemorrhage lagged behind no-reflow, was closely correlated with it, and may be the consequence of microvascular damage.
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