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 ofreperfusion (r=0.88-0.97). This rapid expansion of no reflow predominantly occurred during the first 2 h, finally encompassing similar to80% 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 similar to0.9 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.