ABSTRACT
The early restitution of blood flow to ischemic tissues is essential to halt the progression of cellular injury associated with decreased delivery of oxygen and metabolic substrates, and for removal of potentially harmful metabolic byproducts. However, it is now apparent that reperfusion also initiates a complex series of pathologic events that paradoxically injure tissues. The microcirculation appears to be particularly vulnerable to the deleterious effects of reperfusion in that microvascular dysfunction precedes the development of parenchymal cell injury. When blood flow to certain organs is reinstituted after ischemia, a large proportion of capillaries fail to reperfuse, a phenomenon referred to as capillary no-reflow. Leukocyte/capillary plugging has also been suggested to underlie development of capillary no-reflow in postischemic tissues. While this may contribute to the reduction in capillary perfusion during ischemia, physical impaction of leukocytes within the capillaries does not appear to play a role in the pathogenesis of no-reflow in skeletal muscle when normal perfusion pressures are established at reperfusion.
