Leukocyte--endothelial cell adhesion induced by ischemia and reperfusion.

Reperfusion of ischemic tissues is associated with an enhanced production of inflammatory mediators, increased rolling, adherence, and emigration of leukocytes in postcapillary venules, and vascular protein leakage. There is a growing body of evidence that the leukocyte--endothelial cell interactions are largely responsible for the microvascular dysfunction induced by ischemia--reperfusion. Oxygen radicals, produced by xanthine oxidase and other enzymes, appear to play an important role in initiating and amplifying the inflammatory response elicited by ischemia--reperfusion, while neutrophilic proteases contribute significantly to the injury response. The magnitude of the inflammatory responses observed during ischemia and reperfusion is also influenced by adhesion forces generated by specific glycoproteins expressed on the surface of granulocytes and microvascular endothelium, as well as shear forces that are generated by the movement of blood within the microcirculation. Manipulation of free-radical production, leukocyte--endothelial cell adhesion, and (or) intravascular shear forces provides an effective means for attenuating the deleterious influences of ischemia--reperfusion on the microvasculature.