Microvascular reperfusion injury: rapid expansion of anatomic no reflow during reperfusion in the rabbit

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 · g−1) and plateauing at a level of ∼0.9 ml · min−1 · g−1 by 2 and 8 h of reperfusion (preischemic RMBF: 2.06 ± 0.01 ml · min−1 · g−1). The development of macroscopic hemorrhage lagged behind no reflow, was closely correlated with it, and may be the consequence of microvascular damage.