Microvascular manifestation of postischemic reperfusion injury is hallmarked by two distinct events, i.e. perfusion failure of nutritive capillaries (“no-reflow”) (Majno et al., 1967; Menger et al., 1992a), and the sequelae of “reflow-paradox”-associated mechanisms, which include accumulation of leukocytes, leukocyte-endothelium interaction and loss of endothelial integrity (Menger et al., 1992b). Both reperfusion-dependent events contribute to the aggravation of ischemia-induced parenchymal tissue injury, either through prolongation of focal ischemia (“no-reflow”),or the action of leukocyte-derived cytotoxic mediators (“reflowparadox”),such as reactive oxygen metabolites and proteolytic enzymes (Granger, 1988; Lehr et al., 1991; Menger et al., 1993a).KeywordsLeukocyte AdherenceFocal IschemiaWall Shear RateReactive Oxygen MetabolitePostcapillary VenuleThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.