Early capillary no-reflow during low-flow reperfusion after hind limb ischemia in the rat.

Abstract

Reduction of arterial inflow after ischemia (low-flow reperfusion) is associated with capillary no-reflow and an increase in flap necrosis. The development of these complications may be strongly flow-dependent. The authors wanted to examine the difference between normal-flow and low-flow reperfusion by assessing the gracilis microcirculation with intravital microscopy after 2 hours of hind limb ischemia in the rat. Low-flow reperfusion resulted in capillary no-reflow at an earlier stage compared with normal-flow reperfusion. The capillary lumen was not visible during ischemia and did not open on reperfusion. The authors observed a significant ( <0.05) increase in leukocyte adhesion forces to the postcapillary venules at a later stage of low-flow reperfusion compared with normal-flow reperfusion. However, neither a significant number of adherent leukocytes to the postcapillary venules nor obstruction of capillaries by platelet aggregates could be detected during low-flow reperfusion. Infusion of the protease inhibitor FOY during low-flow reperfusion did not attenuate capillary no-reflow but did reduce leukocyte adhesion forces to the postcapillary venules. Thus, low-flow reperfusion leads to early capillary no-reflow, which may be responsible for further reperfusion damage and flap failure. The mechanism seems to be independent of leukocyte adhesion to the postcapillary venules or platelet aggregation. Instead, endothelial cell and/or tissue swelling in combination with luminal obstruction and leukocyte plugging may be responsible for the early capillary no-reflow phenomenon.