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Articles in PresS, published online ahead of print October 4, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00767.2001
Submitted on August 27, 2001
Accepted on September 26, 2001
1 University of Southern California, The Heart Institute, Good Samaritan Hospital, Los Angeles, California, USA
* To whom correspondence should be addressed. E-mail: ThorstenReffelmann{at}web.de.
No-reflow after acute myocardial infarction is an important predictor of infarct size and clinical outcome. However, the exact relationship between no-reflow and infarct size remains to be determined, in particular as no-reflow may progress during the time course of reperfusion. Control groups of five previous protocols, using the anesthetized, open-chest rabbit model of coronary artery occlusion and reperfusion, were retrospectively analyzed with respect to the correlation between regional myocardial blood flow (RMBF, radioactive microspheres) and infarct size (triphenyltetrazolium chloride) in the course of reperfusion. After 30 minutes of occlusion, reflow (defined as the ratio of RMBF in the risk area divided by the non-ischemic area) declined from hyperemic values after 30 minutes of reperfusion (1.33 ± 0.81, RMBF in the risk area at the same time point: 2.25 ± 1.04 ml/g/min), to 0.47 ± 0.22 after 120 minutes, and 0.46 ± 0.13 after 180 minutes of reperfusion. After 120 minutes of ischemia, reflow at 30 minutes of reperfusion was 0.49 ± 0.24, and deteriorated by 120 minutes of reperfusion (0.26 ± 0.15). In every group, there was a strong correlation between infarct size and reflow (correlation coefficients: -0.62 to -0.82). The lines of regression for the groups with assessment of RMBF after 120 or 180 minutes of reperfusion were nearly identical regardless of the duration of ischemia. Thus, microvascular reperfusion injury led to a striking decrease in RMBF within the first two hours of reperfusion with infarct size as the major determinant of reflow at a given time point of reperfusion.
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